Reviews in cardiovascular medicine最新文献

Background: Current evidence characterizing the association between relative fat mass (RFM) and cardiometabolic disease (CMD) remains limited, with critical gaps persisting in the understanding of age-dependent heterogeneity. Thus, this study aimed to assess the association between RFM and CMD risk across age groups.

Methods: This study utilized data from the China Health Evaluation And Risk Reduction Through Nationwide Teamwork (ChinaHEART), and enrolled 93,801 community-dwelling adults. CMD was defined as a composite diagnosis that included diabetes mellitus, myocardial infarction, and stroke. Meanwhile, RFM was derived from height, waist circumference, and sex. Participants were stratified into groups of young and middle-aged adults (35-59 years) and older adults (≥60 years). Multivariable logistic regression models were employed to estimate odds ratios (ORs) and 95% confidence intervals (CIs), and to test for interaction effects. Restricted cubic spline models were applied to examine dose-response relationships.

Results: Among the 93,801 participants, 18,473 (19.69%) had CMD. In the fully adjusted models, each unit increase in RFM was associated with a 9% increase in CMD risk (OR = 1.09, 95% CI: 1.08-1.09). Compared to the lowest RFM quartile (Q1), higher risks were observed in the Q2 (1.68, 1.59-1.77), Q3 (2.56, 2.34-2.80), and Q4 (4.02, 3.68-4.39) groups (p for trend <0.001). A significant RFM-age interaction was identified (p for interaction = 0.001). Restricted cubic splines confirmed significant non-linear dose-response relationships (both p for overall association <0.001; p for non-linear <0.05), with distinct age-specific patterns. Older adults exhibited higher overall CMD risk compared to young and middle-aged adults. The lower RFM inflection point corresponds to an OR of 1 (30 vs. 34), highlighting the greater vulnerability of this age group and informing the future development of age-specific RFM thresholds.

Conclusions: RFM demonstrates a significant positive association with CMD risk, exhibiting age-dependent heterogeneity, and emphasizing age-tailored interventions for CMD prevention strategies.

Background: Hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) from other causes present similar features on transthoracic echocardiography (TTE), making an accurate differentiation challenging. Recent advancements in radiomics and deep transfer learning (DTL) have shown promise; however, no studies have combined these techniques to diagnose HCM and LVH resulting from other causes. Therefore, we developed a fusion model that integrates radiomic features from the left ventricular myocardium in the four-chamber view of TTE with DTL features to differentiate HCM from other causes of LVH, providing more reliable diagnostic support.

Methods: This multicenter study included 971 patients (303 with HCM, 668 with hypertensive heart disease and uremic cardiomyopathy). Patients from Institution 1 were split into a training set and an internal validation set, while patients from Institution 2 served as an external validation set. Radiomic features were extracted using pyradiomics, and DTL features were obtained via DenseNet121. Features were selected using least absolute shrinkage and selection operator (LASSO) and input into ten machine learning algorithms, with support vector machine (SVM) as the classifier. Model performance was assessed using receiver operating characteristic (ROC) curves and decision curve analysis (DCA) and compared with the diagnostic results of two ultrasound physicians.

Results: The fusion model demonstrated excellent diagnostic performance: the area under the curve (AUC) values were 0.966 (training set), 0.945 (internal validation), and 0.934 (external validation), thereby outperforming models that used only radiomic or DTL features. DCA indicated superior clinical effectiveness, surpassing the diagnostic performance of two ultrasound physicians.

Conclusions: A fusion model combining radiomics and DTL features significantly improves the ability to distinguish HCM from other causes of LVH and has strong potential for clinical applications.

Post-traumatic stress disorder (PTSD), which develops in susceptible individuals after life-threatening or traumatizing events, manifests as a heightened anxiety and startle reflex, disordered sleep, nightmares, flashbacks, and avoidance of triggers. Moreover, PTSD is a predictor and independent risk factor of numerous cardiovascular comorbidities, including stroke, myocardial infarction, coronary atherosclerosis, and atrial fibrillation. Compounding the direct detrimental effects of PTSD on the cardiovascular system, this condition provokes classical cardiovascular risk factors, including high cholesterol and triglycerides, platelet hyperaggregation, endothelial dysfunction, hypertension, and sympathetic hyperactivation. Although most people who have experienced traumatic events do not develop PTSD and are considered PTSD resilient, a substantial minority experience persistent cardiovascular comorbidities. Experimental and clinical studies have revealed a myriad of biomarkers and/or mediators of PTSD susceptibility and resilience, including pro- and anti-inflammatory cytokines, oxidized proteins and lipids, antioxidants, troponin, catecholamines and their metabolites, glucocorticoids, and pro-coagulation factors. The use of biomarkers to predict cardiovascular susceptibility or resilience to PTSD may stratify the risk of a patient developing cardiovascular complications following severe stress. Indeed, since many PTSD biomarkers either inflict or attenuate cardiovascular damage, these biomarkers can be applied to monitor the efficacy of exercise, dietary modifications, and other interventions to enhance cardiovascular resilience and, thereby, restrict the detrimental effects of PTSD on the cardiovascular system. Biomarker-informed therapy is a promising strategy to minimize the risk and impact of cardiovascular diseases in individuals with PTSD.

Background: The clinical value of remnant cholesterol (RC) in patients with in-stent restenosis (ISR) who undergo percutaneous coronary intervention (PCI) is unknown. Therefore, this study aimed to clarify the association between increased RC levels and clinical prognosis in patients with ISR.

Methods: This retrospective study enrolled 836 patients diagnosed with ISR. The study population was divided into four quartiles (Q1-Q4) according to median RC levels. Using a multivariate Cox proportional hazards model and Kaplan-Meier (KM) curve, the association between RC levels and the study endpoint, defined as target-vessel failure (TVF) within 3 years after PCI, was investigated. A discordance analysis was also performed with several definitions.

Results: The KM curve showed an increased risk of TVF with elevated RC levels (p < 0.001). After adjustment, the RC level was identified as an independent predictor of TVF, regardless of whether the metric was considered as a continuous or categorical variable (hazard ratio (HR) = 1.37, 95% confidence interval (CI): 1.16-1.62; p < 0.001; HR = 3.43, 95% CI: 1.85-6.36; p < 0.001). Subgroup analysis showed that the RC-related TVF risk was more pronounced in patients with low-density lipoprotein cholesterol (LDL-C) <1.8 mmol/L (2.75 for each one standard deviation (SD) increase, 95% CI: 1.66-4.55; p for interaction < 0.001). In the discordance analysis, individuals with discordantly high RC levels rather than high LDL-C levels had an increased risk of TVF (HR = 2.02, 95% CI: 1.33-3.07; p < 0.001).

Conclusions: An increased RC level was associated with an elevated risk of TVF in patients with ISR who underwent PCI. Further, the RC-related risk was more pronounced in patients with LDL-C levels <1.8 mmol/L.

Background: We hypothesized that body surface area (BSA)-weighted left ventricular ejection fraction (LVEF) (bLVEF) would represent a superior predictor of mortality in off-pump coronary artery bypass grafting (OPCABG) patients than standard predictors. LVEF is associated with worse outcomes upon OPCABG, while referring left ventricular measurements to BSA should improve predictability.

Methods: The bLVEF was calculated by multiplying the LVEF by the BSA. The primary endpoint was all-cause mortality within 30 days of hospitalization, while secondary endpoints included major postoperative complications.

Results: A total of 7927 patients from five leading cardiac centers participating in the Chinese Cardiac Surgery Registry were included in the final analysis, of which 7093 (89.48%) had normal LVEF, 639 (8.06%) presented heart failure with mid-range ejection fraction (HFmrEF), and 195 (2.46%) exhibited heart failure with reduced ejection fraction (HFrEF). The average bLVEF in the cohort was 109.63 ± 18.16. Both the mortality (odds ratio (OR) 0.97) and secondary endpoints (OR 0.97) followed a similar trend with increasing bLVEF, indicating that bLVEF is a more reliable predictor of adverse outcomes. The individual components of bLVEF, including BSA (area under the curve (AUC) 0.63) and LVEF (AUC 0.64), made minor contributions to mortality risk with relatively low AUC values. However, these components were less impactful than bLVEF (AUC 0.70). Notably, patients with a bLVEF less than 85 had an increased mortality risk relative to those whose bLVEF was 85 or higher (adjusted OR 4.65 (95% confidence interval (CI): 3.81-5.83; p < 0.01)).

Conclusion: The bLVEF serves as a key predictor of mortality in OPCABG patients, effectively eliminating BSA-related bias and demonstrating a strong capacity to predict mortality.

Clinical trial registration: NCT02400125, https://www.clinicaltrials.gov/study/NCT02400125.

Background: This study aimed to identify risk factors for contrast-induced nephropathy (CIN) following rotational atherectomy (RA) in patients with severely calcified coronary lesions to facilitate the prevention of CIN.

Methods: A retrospective analysis was performed on 111 patients who underwent RA in Wuhan Fourth Hospital from July 2021 to June 2023. The creatinine levels of the patients were detected within 48-72 hours after RA, and the patients were divided into a CIN (n = 16) and a non-CIN group (n = 95). Propensity score matching was applied with a caliper value set at 0.02, resulting in 13 matched patient pairs. The risk factors for CIN after RA in these patients were analyzed.

Results: A total of 16 cases of CIN occurred among the 111 patients with coronary heart disease who underwent RA. Following propensity score matching, 13 patients were included in both the CIN and non-CIN groups. The rates of heart failure were significantly higher in the CIN group than those in the non-CIN group before RA (all p < 0.05). However, there was no significant difference in preoperative mean arterial pressure (MAP) between the two groups. Nonetheless, the rate of patients with preoperative MAP <80 mmHg was higher in the CIN group than in the non-CIN group (53.8% vs. 7.7%; p < 0.05). The coronary artery lesion characteristics and interventional treatment strategies were comparable between the two patient groups. Moreover, no statistically significant difference was observed in 1-year major adverse cardiovascular and cerebrovascular events (MACCEs) or secondary endpoint events between the two groups. Logistic regression analysis showed that among the risk factors for CIN after RA, preoperative MAP <80 mmHg (odds ratio (OR) = 17.865, 95% confidence interval (CI): 1.135-281.246) was a risk factor for CIN (p < 0.05).

Conclusion: Patients with a preoperative MAP below 80 mmHg are at increased risk of CIN following RA. This cohort requires intensive monitoring to prevent CIN, ensuring prompt implementation of management strategies to avert CIN onset and mitigate the adverse effects of CIN post-RA treatment.

Tuberculosis (TB) is a contagious disease caused by Mycobacterium tuberculosis (M. tuberculosis) and is transmitted through airborne particles. Although TB usually damages the lungs, this disease can also cause complications in various organs, including the cardiovascular system. Indeed, pericarditis represents the most frequently reported cardiac manifestation of TB, and may present alongside fever, dyspnea, cough, or increased central venous pressure, hepatomegaly, and peripheral edema. Tuberculous-related pericarditis treatment is challenging due to the poor penetration of anti-tuberculous drugs into the pericardium. Myocarditis is another form of cardiac manifestation and is often associated with arrhythmias. Tuberculous aortitis typically causes dilatation leading to pseudoaneurysm formation and is usually asymptomatic; however, this manifestation can result in sepsis, aortic rupture, or even death, although rarely. Cardiac tuberculomas may present with general symptoms and can impair heart function by obstructing the outflow tracts, leading to ventricular dysfunction. Additionally, the primary treatment of TB carries cardiotoxicity risks, such as various arrhythmias. Moreover, TB significantly increases the risk of cardiovascular conditions, including myocardial infarction and coronary artery obstruction. Therefore, early recognition and a multidisciplinary approach are crucial to prevent severe outcomes such as sudden cardiac death, sepsis, or aortic rupture. Thus, this review highlights the spectrum of TB-related cardiac complications and underscores the importance of greater awareness and timely multidisciplinary care.

This review aims to summarize the status and future directions of pediatric heart failure (HF) pharmacotherapy. Notably, managing HF in children presents unique challenges due to heterogeneous etiologies and a longstanding paucity of pediatric-specific data. While historically reliant on adult-derived evidence, current treatment strategies are evolving through an integration of novel and pediatric-focused therapies. Indeed, present pediatric HF algorithms, adapted from adult guidelines, now include four pharmacologic pillars: angiotensin-converting enzyme (ACE) inhibitors/angiotensin receptor blockers/angiotensin receptor-neprilysin inhibitors (ARNIs), β-blockers, mineralocorticoid receptor antagonists, and sodium-glucose cotransporter-2 (SGLT2) inhibitors. Multicenter registries, such as the Pediatric HF Registry, the Pediatric Cardiomyopathy Registry (PCMR), and the Advanced Cardiac Therapies Improving Outcomes Network (ACTION) HF medication titration projects, are further shaping a more evidence-informed and personalized approach. A comprehensive literature search was conducted using PubMed, Scopus, and Google Scholar to identify recent review articles, clinical trials, and guideline documents relevant to pediatric HF pharmacotherapy. The search focused on articles published in the English language from the past decade, with particular attention to transformative therapeutic insights. Data from adult HF studies were also included to provide context and bridge gaps in pediatric evidence. Where available, pediatric-specific data were prioritized to inform applicability. Relevant findings were critically appraised, synthesized, and integrated to develop a cohesive narrative reflecting current trends and emerging directions in pharmacological management of pediatric HF. This review examined the evolving landscape of medical therapies for chronic pediatric HF, underscoring the limitations of a one-size-fits-all approach. The heterogeneity of underlying etiologies complicates the development of guideline-directed treatments tailored to children, particularly when attempting to stratify care by phenotypes such as heart failure with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF), as is commonly practiced in adult populations. There is an urgent need to individualize treatment strategies based on the hemodynamic profile of each pediatric patient, advocating for the integration of precision-based care into guideline-directed medical therapy. Such an approach not only enhances clinical outcomes in a population marked by etiologic diversity and developmental variability but also informs scalable care models and future guideline frameworks that reflect the unique needs of children with HF.

To accumulate and evaluate current evidence on bleeding complications associated with antiplatelet therapy and the specific contributions of pharmacists and nurses to bleeding-risk mitigation. Antiplatelet agents prevent arterial thrombosis by inhibiting platelet aggregation through blocking cyclooxygenase-1, P2Y₁₂ receptors, glycoprotein (GP) IIb/IIIa receptors, or phosphodiesterase pathways. These mechanisms simultaneously impair primary hemostasis, increasing the risk of intracranial, gastrointestinal, or other clinically significant bleeding. Bleeding risk is dose-, duration-, and drug-dependent; meanwhile, dual antiplatelet therapy (DAPT) and concurrent use of anticoagulants, non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or proton pump inhibitors all amplify the risk. Patient-specific factors, likely older ages, anemia, renal or hepatic impairment, prior bleeding, cancer, diabetes, and frailty further increase the hazard. Shortened DAPT or P2Y₁₂ inhibitor monotherapy reduces bleeding without increasing thrombotic events. Pharmacists optimize regimens, screen for interactions, educate patients, and co-develop institutional protocols; nurses monitor early signs of bleeding, ensure adherence, and coordinate multidisciplinary care. Both roles demonstrably decrease the incidence and severity of bleeding. Individualized antiplatelet strategies, guided by refined risk-stratification tools and delivered through pharmacist-nurse integrated care models, can maximize antithrombotic benefit while minimizing bleeding harm. Thus, large prospective trials and cost-effectiveness analyses are warranted to validate these multidisciplinary interventions.

Transcatheter aortic valve replacement (TAVR) has revolutionized the treatment landscape for severe symptomatic aortic stenosis among all surgical risk groups. Thus, following the expansion of TAVR use and constant improvements in TAVR platforms and implantation techniques, implementation has been extended to special population groups that were previously underrepresented in clinical trials. This review evaluates the role of TAVR in patients with unique clinical considerations, including those with active malignancies, psychiatric disorders, and advanced organ dysfunction. By examining current literature, we provide insights into the safety, efficacy, appropriateness, and specific challenges associated with TAVR in these patient groups.