Calcium signaling abnormality in cardiomyocytes, as a key mechanism, is closely associated with developing heart failure. Fibroblast growth factor 13 (FGF13) demonstrates important regulatory roles in the heart, but its association with cardiac calcium signaling in heart failure remains unknown. This study aimed to investigate the role and mechanism of FGF13 on calcium mishandling in heart failure. Mice underwent transaortic constriction to establish a heart failure model, which showed decreased ejection fraction, fractional shortening, and contractility. FGF13 deficiency alleviated cardiac dysfunction. Heart failure reduces calcium transients in cardiomyocytes, which were alleviated by FGF13 deficiency. Meanwhile, FGF13 deficiency restored decreased Cav1.2 and Serca2α expression and activity in heart failure. Furthermore, FGF13 interacted with microtubules in the heart, and FGF13 deficiency inhibited the increase of microtubule stability during heart failure. Finally, in isoproterenol-stimulated FGF13 knockdown neonatal rat ventricular myocytes (NRVMs), wildtype FGF13 overexpression, but not FGF13 mutant, which lost the binding site of microtubules, promoted calcium transient abnormality aggravation and Cav1.2 downregulation compared with FGF13 knockdown group. Generally, FGF13 deficiency improves abnormal calcium signaling by inhibiting the increased microtubule stability in heart failure, indicating the important role of FGF13 in cardiac calcium homeostasis and providing new avenues for heart failure prevention and treatment.

Chronic total occlusion (CTO) poses a significant challenge in cardiovascular interventional therapy, owing to the complexity and difficulty involved, which limit the effectiveness of traditional treatment methods. Thus, innovative designs and application concepts of guidewires have expanded the possibilities for clinical intervention, resulting in significant improvements in treatment strategies for CTO. Recently, numerous studies have detailed the application experiences of various guidewires in CTO interventional therapy, including the performance characteristics, selection strategies, and differences in clinical outcomes. Nevertheless, despite these advancements, limitations remain in CTO treatment, such as low success rates and the risk of complications. Therefore, this article aims to review the current application experience of CTO guidewires. Moreover, by reviewing existing literature and summarizing clinical practices, this paper explores strategies to optimize guidewire selection and usage to enhance the success rate and safety of CTO interventional therapy and provide practical guidance for clinicians.

Coronary artery calcification (CAC) increases the risk of acute coronary syndrome. This study examined the correlation between C1q/TNF-related protein 9 (CTRP9) and CAC and explored CTRP9 as a biomarker for prognosis. We divided 275 patients with coronary heart disease into four groups. In order to balance the baseline confounding factors, propensity score matching (PSM) was performed to match CAC patients with non-CAC patients in a 1:1 ratio. Optical coherence tomography (OCT) calcification scoring was performed in 126 patients with CAC. Moreover, 140 patients who underwent OCT were followed-up for 9 months for analysis of the correlation between CTRP9 levels and clinical prognosis. Based on OCT calcification scores, 126 patients with CAC were divided into the 0–2 and 3–4 groups. Plasma CTRP9 levels were significantly lower in the type 2 diabetes mellitus (T2DM), CAC and CAC with T2DM groups than in the control group. CTRP9 played roles as a protective factor and potential predictor in CAC severity. The AUC of the OCT calcification score 3–4 group predicted by the plasma CTRP9 level was 0.766. During the follow-up period, the cumulative event-free survival rate was significantly lower in the low-level CTRP9 (L-CTRP9) group than in the high-level (H-CTRP9) group, and the incidence of major endpoint events was significantly higher in the L-CTRP9 group than in the H-CTRP9 group. CTRP9 can be a valuable biomarker for CAC occurrence and severity and can predict patients’ clinical prognosis.

Ventricular arrhythmia (VA) is one of the common complications of many heart diseases in clinical practice, even some of its clinical symptoms are mild and non-specific, but the other may lead to sudden cardiac death (SCD) and most life-threatening VA is associated with ischemic cardiomyopathy (ICM). Nowadays, the developments in imaging techniques have provided clues to identify these highly variable VAs, which make clinicians identify patients with VA early and effectively who may have fatal consequences. Thereafter, it is beneficial to manage the risk stratification of patients, optimize their follow-up treatment, and improve clinical outcomes. This article reviews current ultrasound and magnetic resonance imaging techniques that can aid in diagnosis, treatment and prognosis, and provides clinicians with practical imaging and analytical recommendations to further identify patients with ICM who may develop VA. Clinical trial number Not applicable.

Background: Vascular calcification predicts adverse cardiovascular outcomes. CTRP9, an adiponectin paralog, has vascular protective effects. We evaluated the association of circulating CTRP9 with aortic valve calcification (AVC) and coronary artery calcification (CAC) in a cross-sectional observational study. Methods: Nine hundred coronary heart disease patients underwent echocardiography and optical coherence tomography; serum CTRP9 was measured in a subset. Logistic regression identified CAC determinants. ROC analysis assessed CTRP9 alone and combined with AVC for predicting severe CAC. AVC was modeled in ApoE−/− mice fed a Western diet for 24 weeks, with calcification markers analyzed via PCR and Western blot. Results: CTRP9 independently protected against CAC (OR = 0.156, 95% CI: 0.11–0.21, p < 0.05). CTRP9 predicted CAC severity (AUC = 0.74), and combining it with AVC improved prediction of severe CAC (AUC = 0.843). Kendall’s Tau-b indicated strong correlation between severe AVC and CAC (τb = 0.597, p < 0.001). Exogenous CTRP9 attenuated aortic valve calcification in mice. Conclusion: Lower CTRP9 levels associate with advanced AVC and greater CAC severity. Combining CTRP9 with AVC enhances risk prediction, highlighting CTRP9 as a potential biomarker and therapeutic target in vascular calcification.