Circulation Journal最新文献

Background: Passive leg lifting (PLL) may serve as a simple alternative to simulate exercise stress.

Methods and results: We evaluated 33 patients with PH who underwent PLL-RHC and exercise right heart catheterization (RHC); 25 patients were classified as having PLL-induced PH (LIPH), demonstrating significant increases in mean pulmonary arterial pressure (mPAP) and mPAP-cardiac output slopes. Strong correlations were observed between PLL-RHC and exercise RHC measurements.

Conclusions: PLL-RHC may represent a simple method for detecting EIPH.

Background: Cardiovascular autonomic neuropathy (CAN) is a major complication of type 2 diabetes mellitus (T2DM), but the roles of arterial stiffness and right atrial (RA) function in CAN remain unclear.

Methods and results: In 120 patients with T2DM, we assessed short-term heart rate variability (CVR-R), cardio-ankle vascular index (CAVI), and two-dimensional speckle-tracking echocardiography (2DSTE). CAN was defined as CVR-R <2%. Multivariable analysis showed that higher CAVI and lower RA function composite scores were independently associated with CAN.

Conclusions: Both increased arterial stiffness and impaired RA function characterized CAN, indicating a key cardiovascular interaction. Combined CAVI and RA strain assessment may aid early detection.

Background: In repaired tetralogy of Fallot (TOF) and related diseases, reoperation for pulmonary regurgitation (PR) may be delayed unless marked right ventricular (RV) enlargement is present.

Methods and results: 32 patients with significant PR post-repair underwent catheterization and 4D flow MRI for reoperation evaluation. The Non-severe RV Dilation group (n=20) did not meet the surgical volume criteria, whereas the Severe RV Dilation group (n=12) did. The Non-severe RV Dilation group had higher biventricular filling pressures. The RV-Energy loss index in both groups was high.

Conclusions: Diastolic dysfunction could serve as a therapeutic target in PR patients with heterogeneous etiologies.

Cardiac conduction is a central determinant of normal rhythm and arrhythmia susceptibility. Although arrhythmias have traditionally been attributed to abnormal automaticity, triggered activity, and re-entry, emerging evidence indicates that conduction abnormalities integrate structural, electrical, and immune-derived signals into a common arrhythmogenic substrate. This review summarizes multiscale mechanisms of impulse propagation, with an emphasis on gap junction-mediated coupling. Connexin 43 (Cx43), the principal ventricular connexin, maintains intercellular current flow through phosphorylation-dependent localization at intercalated discs; its remodeling leads to conduction slowing, heterogeneous propagation, and reentrant vulnerability. Recent studies have revealed that cardiac resident macrophages preserve ventricular conduction by promoting Cx43 phosphorylation via amphiregulin-epidermal growth factor receptor signaling. Loss of this macrophage-derived pathway causes Cx43 disorganization, atrioventricular block, ventricular fibrillation, and sudden death during cardiac stress, establishing an immune-electrical interface essential for conduction stability. This review further highlights conduction abnormalities in human disease, differences between mice and humans, and insights derived from electrocardiography and advanced computational modeling. Simulations linking molecular alterations to organ-level activation patterns provide a mechanistic bridge between cellular coupling, Purkinje network integrity, fibrosis distribution, and clinical electrophysiology. Together, these findings position conduction as a dynamic, regulated property of the ventricular myocardium and suggest that targeting gap junction and immune pathways may enable future conduction-based precision cardiology.

Background: Ischemic heart disease remains the leading cause of death worldwide, and although early coronary revascularization is essential, it can paradoxically induce additional myocardial damage known as ischemia-reperfusion (I/R) injury, driven in part by excessive generation of reactive oxygen species (ROS). This study evaluated the cardioprotective potential of resorcimoline (RML), a newly developed free radical scavenger, in mitigating ROS-mediated myocardial injury in a preclinical setting.

Methods and results: ROS production was induced in primary cardiomyocytes through hypoxia, angiotensin II, or hydrogen peroxide treatment. The antioxidant effects of RML were assessed by cytosolic and mitochondrial ROS assays. Cell viability and cytotoxicity were evaluated by metabolic activity and lactate dehydrogenase release assays. In vivo, myocardial I/R injury was induced in rats by transient coronary artery ligation followed by reperfusion. RML significantly reduced intracellular and mitochondrial ROS levels and improved cardiomyocyte viability in vitro. Consistently, in vivo DHE staining demonstrated that RML suppressed myocardial ROS accumulation, decreased infarct size, lowered serum troponin I, reduced apoptosis, and preserved left ventricular function, whereas these protective effects were not observed without reperfusion.

Conclusions: RML exerts cardioprotective effects by scavenging ROS and mitigating downstream oxidative damage in both in vitro and in vivo models of myocardial I/R injury, suggesting promise as a therapeutic agent against reperfusion-induced myocardial injury.