Cardiovascular Therapeutics最新文献

Background: In cardiogenic shock (CS), titration of both the choice and dosage of inotropes and vasopressors is crucial. The vasoactive-inotropic score (VIS) quantifies hemodynamic support, while the effect of temporal VIS change on prognosis remains unclear. This study evaluated the association between the vasoactive-inotropic score reduction rate (VRR) to measure VIS changes over time and explore its association with mortality in CS patients.

Methods: We performed a retrospective observational study using two large intensive care databases (MIMIC-IV and eICU). Adult patients with CS receiving vasoactive-inotropic agents within 24 h after ICU admission were included. VIS was calculated using the updated VIS 2020, and VRR was defined to capture the relative change in VIS over time. Patients were categorized into VIS-decreasing and VIS-increasing groups. The primary outcome was in-hospital mortality; secondary outcomes were intensive care unit (ICU) and 28-day mortality (28-day mortality only for the MIMIC-IV database). Associations between VRR and outcomes were examined using four models: (1) log-rank analysis, (2) Cox model adjusted for all covariates, (3) Cox model adjusted for covariates selected by univariable analyses, and (4) Cox model adjusted for covariates selected by a random forest algorithm.

Results: A total of 3170 adult CS patients were analyzed. All models in both MIMIC-IV and eICU showed that an increasing VIS over time was consistently associated with higher in-hospital, ICU, and 28-day mortality compared with a decreasing VIS in the MIMIC-IV cohort (p < 0.001). These findings were reproduced in the external eICU cohort for ICU and in-hospital mortality (p < 0.001), supporting the robustness and generalizability of VRR as a prognostic indicator across heterogeneous ICUs.

Conclusions: In adult CS patients, a greater reduction in VIS over time is strongly associated with lower mortality. VRR provides a simple, dynamic summary of vasoactive trajectories and may serve as a useful adjunct for risk stratification alongside other clinical and biochemical markers, although prospective validation is warranted.

Objective: Environmental exposure to metals is recognized as a significant trigger of chronic inflammation and various systemic diseases, with inflammatory processes playing a central role in the development and progression of CKM syndrome. The MMII, which integrates multiple metal exposures and inflammatory responses, has demonstrated sensitivity in predicting population health risks. However, its association with all-cause mortality in individuals with CKM Stages 0-3 has not been previously investigated.

Methods: This study analyzed publicly available data from the NHANES 1999-2010, including adults aged 20 years and older with CKM syndrome Stages 0-3. The MMII was constructed based on urinary concentrations of heavy metals (mercury, cadmium, cobalt, molybdenum, lead, and tungsten) along with C-reactive protein and white blood cell count. The primary outcome was all-cause mortality. Cox proportional hazards regression models were employed to assess the association between MMII and all-cause mortality, with sequential adjustment for potential confounders, complemented by sensitivity and subgroup analyses.

Results: The final analysis included 2643 participants (mean age: 44.24 years; 56.77% female). Higher MMII levels were significantly associated with increased all-cause mortality. In the fully adjusted model, participants in the highest MMII quartile exhibited a hazard ratio (HR) for all-cause mortality of 1.50 (95% CI: 1.01-2.22, p = 0.04). Restricted cubic spline analysis revealed a nonlinear dose-response relationship between MMII and mortality risk (P for nonlinearity = 0.007). Threshold effect analysis identified an inflection point at MMII = 0.10594.Threshold effect analysis identified an inflection point at MMII = 0.10594. Below this threshold, the association between MMII and all-cause mortality was not statistically significant, with a point estimate below 1 and wide confidence intervals (HR: 0.554, 95% CI: 0.171-1.795). Above the threshold, higher MMII was associated with greater mortality risk (HR: 3.977, 95% CI: 1.777-8.901). Sensitivity analyses yielded consistent results. Subgroup analysis revealed a significant interaction between MMII and age group for mortality risk (p < 0.05).

Conclusions: In the U.S. population with CKM Stages 0-3, MMII is significantly associated with all-cause mortality. These findings highlight the importance of the inflammatory burden resulting from multiple metal exposures as a significant risk factor for all-cause mortality in early-stage CKM syndrome, underscoring the need for environmental health management and integrated approaches to chronic disease prevention.

Objectives: Postoperative atrial fibrillation (POAF) is a common complication after off-pump coronary artery bypass grafting (OPCABG) and contributes to increased morbidity and prolonged hospital stays. Both myocardial ischemia and systemic inflammation play a critical role in its pathogenesis, which is closely related to the intensity of coronary revascularization and antiplatelet treatment, respectively.

Methods: This study investigated the impact of the interaction between completeness of coronary revascularization and antiplatelet regimen on POAF incidence.

Results: A total of 505 eligible patients, undergoing elective first-time OPCABG surgery from May 2017 to May 2024, were reviewed and divided into the incomplete revascularization (IR) group (n = 143) and complete revascularization (CR) group (n = 362) according to the extent of coronary revascularization. The incidence of POAF within the first week post-OPCABG was 39.2% in the IR group versus 25.1% in the CR group (hazard ratio [HR]: 1.70, 95% confidence interval [CI]: 1.18-2.46; p = 0.002). AF burden (10.1% [IQR 4.8%, 16.5%] vs. 6.0% [IQR 2.3%, 9.5%], p = 0.003), inflammatory markers (interleukin-6 [IL-6] on Day 1: 104 ± 20 vs. 98 ± 16 pg/mL, p < 0.001), markers of prothrombotic state (D-dimer on Day 5: 2.6 ± 0.7 mg/L FEU vs. 2.3 ± 0.7 mg/L FEU, p < 0.001), and postoperative hospital stay (10.7 ± 1.8 vs. 10.3 ± 1.8 days, p = 0.006) were significantly higher in the IR group compared to the CR group. Among patients receiving clopidogrel, POAF incidence was 42.6% (IR) vs. 25.9% (CR) (p = 0.001). Among patients receiving ticagrelor, POAF incidence was 25.0% (IR) vs. 22.5% (CR).

Conclusion: IR was associated with a higher rate of POAF after OPCABG in patients receiving clopidogrel-based DAPT, but not in those receiving ticagrelor-based DAPT.

Aim: The aim of this study is to share our experience of the combined double-orifice and single-patch technique for the correction of partial atrioventricular septal defect (pAVSD) and its associated tricuspid valve dysplasia (TVD).

Methods: Between January 2014 and May 2024, 99 patients (age ≥ 18 years) who underwent repair of pAVSD and its associated TVD using the aforementioned strategy were retrospectively analyzed.

Results: The mean aortic cross-clamp time was 48.5 ± 12.6 min, and the mean cardiopulmonary bypass time was 75.8 ± 13.0 min. Follow-up was 100% at a mean of 5.2 years (3-8 years). No operative or late deaths occurred. No evidence of mitral stenosis was detected, and only one patient developed a severe MR 2 years after the surgery and underwent reoperation. There was no moderate or severe tricuspid regurgitation during follow-up. There was neither secondary tricuspid valve repair nor permanent pacemaker implantation among all patients.

Conclusions: The combined double-orifice and single-patch technique is a safe, effective, and durable strategy for repair of pAVSD and its associated TVD, demonstrating an excellent technical reproducibility.

W. Li, D. Wang, C. Lin, et al., “A Meta-Analysis of the Incidence of Adverse Reactions of Statins in Various Diseases,” Cardiovascular Therapeutics 2025, no. 1 (2025): 1–29, https://doi.org/10.1155/cdr/6684099.

In the article titled “A Meta-Analysis of the Incidence of Adverse Reactions of Statins in Various Diseases,” incorrect funding details were included.

The correct funding statement should read:

This work was funded by the Fifth Batch of National Outstanding Traditional Chinese Medicine Clinical Talent Cultivation Program (National Administration of Traditional Chinese Medicine, Document No. [2022] 239) and the Guangxi First-Class Discipline Construction Project (Gui Jiao Ke Yan [2022] No. 1).

We apologize for this error.

In the realm of cardiovascular diseases, myocardial ischemia–reperfusion injury (MIRI) is known as one of the main life-threatening conditions with significant morbidity and mortality. Although some therapeutic approaches, like pharmacological treatments and ischemic preconditioning, have been suggested for MIRI, offering a functional approach with high effectiveness for MIRI remains challenging. Recent studies have indicated that oxycodone, a semisynthetic opioid used to improve acute to chronic pain, may be cardioprotective against MIRI. The current experimental evidence showed that these protective influences can stem from the ability of oxycodone to regulate apoptosis, inflammation, and oxidative stress, as well as promote cardiovascular parameters (e.g., infarct size, cardiac function, and endothelial integrity). Hence, the main purpose of this narrative review study is to summarize and discuss the anti-MIRI potential of oxycodone with a mechanistic insight. This narrative review was also conducted to hold promise for researchers and clinicians to consider and assess its clinical capacity for subjects suffering from this challenging disease.

Severe thermal burns involving ≥ 20% of total body surface area (TBSA) initiate a distinct, prolonged physiological cascade extending well beyond the acute phase. This dysregulated response features chronic hypermetabolism, lipid remodeling, and sustained cardiovascular stress. While survival has improved with advances in acute care, the long-term cardiometabolic effects, particularly the link between lipid abnormalities and cardiovascular risk, remain underexplored. This review highlights the complex pathophysiology of burn-induced hypermetabolism, including elevated resting energy expenditure, catecholamine-driven lipolysis, mitochondrial uncoupling, and maladaptive adipose browning. Even in metabolically healthy individuals, these mechanisms promote atherogenic dyslipidemia, characterized by hepatic steatosis, elevated small-dense LDL, reduced HDL-C, and persistent hypertriglyceridemia. Emerging lipidomic and clinical data correlate these changes with increased Framingham risk scores, systemic inflammation, and TBSA extent. Simultaneously, cardiovascular vulnerability increases due to myocardial remodeling, autonomic dysfunction, and vascular impairment, particularly in young survivors with prolonged metabolic responses. Imaging and metabolomics reveal endothelial injury, subclinical cardiac dysfunction, and elevated arrhythmogenic risk persisting years after healing. We evaluate current interventions, β-blockers, omega-3 fatty acids, statins, anti-inflammatory agents, and structured rehabilitation, within a multimodal framework. Additionally, we identify critical gaps, including the need for precision metabolic modulation, omics-based monitoring, and tailored cardiovascular risk algorithms. Recognizing severe burns as systemic illnesses with delayed but measurable cardiovascular consequences requires a paradigm shift in long-term care. This review advocates for proactive, multidisciplinary cardiometabolic surveillance as an essential component of postburn recovery. This review follows the TITAN 2025 guideline for transparency in research and reporting.¹