Journal of Cardiovascular Development and Disease最新文献

Background: Vascular aging (VA) reflects arterial biological aging and is closely linked to cardiovascular risk. Carotid-femoral pulse wave velocity (cfPWV) is the gold standard for assessing arterial stiffness and VA. However, evidence is limited on cfPWV-derived vascular age and its association with subclinical target organ damage (TOD) in the general population. This study evaluated whether Δ-age (vascular age minus chronological age) could identify individuals at higher risk of early vascular injury in a Chinese community cohort.

Methods: This cross-sectional study included participants from two Beijing communities. Δ-age was calculated as cfPWV-derived vascular age minus chronological age. Participants were categorized as supernormal vascular aging (SUPERNOVA, <10th percentile), normal VA, and early vascular aging (EVA, 90th percentile). TOD included mean and maximum carotid intima-media thickness (CIMT), and carotid plaque. Associations between Δ-age and TOD were analyzed using multivariable regression models adjusted for conventional cardiovascular risk factors and cfPWV.

Results: A total of 6305 participants (mean age 62.5 ± 7.8 years; 34.2% male) were included. Higher Δ-age was associated with increased mean and maximum CIMT and higher carotid plaque prevalence, independent of cfPWV. EVA participants had a higher risk, whereas SUPERNOVA participants had a lower risk of TOD compared with normal VA. After cfPWV adjustment, EVA remained associated with increased mean CIMT and carotid plaque, while SUPERNOVA showed a nonsignificant trend toward a lower risk. Associations were consistent across subgroups.

Conclusions: Δ-age, independent of cfPWV, was an independent risk factor for TOD. This simple, practical indicator may help identify individuals at risk of early vascular damage in community settings.

Background: Structural and functional adaptation of the heart to chronic exercise is dependent on multiple factors, including the volume and type of training, and has direct implications for pre-participation cardiac screening (PPCS). Sailing is a unique multi-training modality sport with limited prior description of cardiac adaptation to training. The aims of this study are (1) to describe electrocardiogram (ECG) changes in sailors, informing PPCS guidelines; (2) to assess structural and functional cardiac changes in sailors; and (3) to examine sex- or discipline-specific cardiac adaptations in sailors. Methods: Seventy elite sailors (33 females) underwent standard ECG and echocardiography. Echocardiographic data were compared to population norms and analysed by sex and sailing discipline based on training type: isometric (IG), pumping (PG), and movement (MG). Results: One sailor presented with abnormal ECG findings (T wave inversion) which warranted further investigation. Primary training-related ECG changes noted were early repolarisation (24%) and sinus bradycardia (30%). The left ventricular volume index was dilated in 18% of all sailors compared to reference values, with similar findings noted on right ventricular parameters for 22% of the study population, although in males only. The impact of predominant training stimulus (IG, PG, MG) did not mediate differences in the structure of any cardiac chambers (p > 0.05). Ejection fraction was lower in the PG (Δ4%, p ≤ 0.001), whereas global longitudinal strain was higher (Δ2%, p = 0.02) compared to MG and IG. Conclusions: Elite-level sailors present with electrical and structural cardiac phenotypes associated with exercise adaptation, with dilation of both left- and right-sided chambers. These data should be considered when interpreting results of PPCS in male and female sailors from different, specific disciplines.

Background: Insulin resistance (IR) has been implicated in cardiovascular diseases, and a correlation between IR and the slow flow phenomenon (CSF)has been identified. The triglyceride-glucose index (TGI), a simple surrogate marker for IR, has recently emerged as a potential predictor of CSF, though data are limited. The aim of this study was to evaluate the association of TGI and other prognostic parameters in patients with CSF.

Methods: This retrospective study included 693 patients who underwent diagnostic coronary angiography between January 2022 and December 2024. A total of 132 patients were diagnosed with CSF based on the corrected TIMI frame count (cTFC > 27 in at least one epicardial coronary artery), while 561 patients had normal coronary flow (NCF). Patients with confounding cardiovascular or systemic conditions were excluded. Clinical, demographic, and laboratory data were gathered, and TGI was calculated as ln [fasting triglycerides (mg/dL) × fasting glucose (mg/dL)/2].

Results: Statistically significant distinctions were found between the CSF and NCF groups regarding TGI, age, glucose, HbA1c, creatinine, sodium, CRP, platelet count, heart rate, PR interval, and cQT interval (p < 0.05). Age, hypertension, diabetes mellitus, HbA1c, glucose, sodium, and cQT were identified as potential clinical and laboratory factors associated with CSF in univariate logistic regression analysis; however, no independent predictor was found in multivariate analysis. ROC analysis showed that a TGI cut-off value of ≥8.93 predicted CSF with 67.6% sensitivity and 66.7% specificity.

Conclusions: Our study demonstrated that TGI was significantly greater in patients with CSF compared to those with NCF. Although TGI showed limited sensitivity and specificity in discriminating CSF, its possible value as a prognostic indicator warrants further validation in prospective, large-scale studies.

Cardiogenic pulmonary edema (CPE) is a life-threatening manifestation of acute heart failure characterized by rapid accumulation of fluid in the interstitial and alveolar spaces, leading to severe dyspnea, hypoxemia, and respiratory failure. The condition arises from elevated left-sided filling pressures that increase pulmonary capillary hydrostatic pressure, disrupt alveolo-capillary barrier integrity, and impair gas exchange. Neurohormonal activation further perpetuates congestion and increases myocardial workload, creating a vicious cycle of hemodynamic overload and respiratory compromise. Respiratory support is a cornerstone of management in CPE, aimed at stabilizing oxygenation, reducing the work of breathing, and facilitating ventricular unloading while definitive therapies, such as diuretics, vasodilators, inotropes, or mechanical circulatory support (MCS), address the underlying cause. Among available modalities, non-invasive ventilation (NIV) with continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP) has the strongest evidence base in moderate-to-severe CPE, consistently reducing the need for intubation and providing rapid relief of dyspnea. High-flow nasal cannula (HFNC) represents an emerging alternative in patients with moderate hypoxemia or intolerance to mask ventilation, and should be considered an adjunctive option in selected patients with less severe disease or NIV intolerance, although its efficacy in severe presentations remains uncertain. Invasive mechanical ventilation is reserved for refractory cases, while extracorporeal membrane oxygenation (ECMO) and other advanced circulatory support modalities may be necessary in cardiogenic shock. Integration of respiratory strategies with hemodynamic optimization is essential, as positive pressure ventilation favorably modulates preload and afterload, synergizing with pharmacological unloading. Future directions include personalization of ventilatory strategies using advanced monitoring, novel interfaces to improve tolerability, and earlier integration of MCS. In summary, respiratory support in CPE is both a bridge and a decisive therapeutic intervention, interrupting the cycle of hypoxemia and hemodynamic deterioration. A multidisciplinary, individualized approach remains central to improving outcomes in this high-risk population.

Understanding thrombosis in acute coronary syndromes (ACSs) has evolved through advances in biomarkers, intracoronary imaging, and emerging analytical tools, improving diagnostic accuracy and risk stratification in high-risk patients. This narrative review provides an integrative overview of contemporary evidence from clinical trials, meta-analyses, and international guidelines addressing circulating biomarkers, intracoronary imaging modalities-including optical coherence tomography (OCT), intravascular ultrasound (IVUS), and near-infrared spectroscopy (NIRS)-artificial intelligence-based analytical approaches, and emerging antithrombotic therapies. High-sensitivity cardiac troponins and natriuretic peptides remain the most robust and guideline-supported biomarkers for diagnosis and prognostic assessment in ACS, whereas inflammatory markers and multimarker strategies offer incremental prognostic information but lack definitive validation for routine therapeutic guidance. Intracoronary imaging with IVUS or OCT is supported by current guidelines to guide percutaneous coronary intervention in selected patients with ACS and complex coronary lesions, leading to improved procedural optimization and clinical outcomes compared with angiography-guided strategies. Beyond procedural guidance, OCT enables detailed plaque characterization and mechanistic insights into ACS, while NIRS provides complementary information on lipid-rich plaque burden, primarily for risk stratification based on observational evidence. Artificial intelligence represents a rapidly evolving tool for integrating clinical, laboratory, and imaging data, with promising results in retrospective and observational studies; however, its clinical application in thrombosis management remains investigational due to the lack of outcome-driven randomized trials. In the therapeutic domain, factor XI inhibitors have demonstrated favorable safety profiles with reduced bleeding and preserved antithrombotic efficacy in phase II and early phase III studies, but their definitive role in ACS management awaits confirmation in large, outcome-driven randomized trials. Overall, the integration of biomarkers, intracoronary imaging, and emerging analytical and pharmacological strategies highlights the potential for more individualized cardiovascular care. Nevertheless, careful interpretation of existing evidence, rigorous validation, and alignment with guideline-directed practice remain essential before widespread clinical adoption.

Background: There exists some inconsistent evidence on the relationship between altered cardiac morphology, its function, and frailty. Therefore, this study aimed to assess the associations among frailty, lean body mass, central arterial stiffness, and cardiac structure and geometry in older people with a normal ejection fraction. Methods: A total of 205 patients >65 years were enrolled into this ancillary analysis of the FRAPICA study and were assessed for frailty with the Fried phenotype scale. Left ventricular dimensions and geometry were assessed with two-dimensional echocardiography. Fat-free mass was measured using three-site skinfold method. Parametric and non-parametric statistics and analysis of covariance were used for statistical calculations. Results: Frail patients were older and women comprised the majority of the frail group. Frail men and women had comparable weight, height, fat-free mass, blood pressure, central blood pressure, and carotid-femoral pulse wave velocity to their non-frail counterparts. There was a linear correlation between the sum of frailty criteria and left ventricular end-diastolic diameter (Spearman R = -0.17; p < 0.05) and relative wall thickness (Spearman R = 0.23; p < 0.05). In the analysis of covariance, frailty and gender were independently associated with left ventricular mass (gender: β of -0.37 and 95% CI of -0.50--0.24 at p < 0.001), the left ventricular mass index (gender: β of -0.23 and 95% CI of -0.37--0.09 at p < 0.001), and relative wall thickness (frailty: β of -0.15 and 95% CI of -0.29--0.01 at p < 0.05; gender: β of 0.23 and 95% CI of 0.09-0.36 at p < 0.01). Frailty was associated with a shift in heart remodeling toward concentric remodeling/hypertrophy. Conclusions: Frailty is independently associated with thickening of the left ventricular walls and a diminished left ventricular end-diastolic diameter, which are features of concentric remodeling or hypertrophy. This association appears to be more pronounced in women. Such adverse cardiac remodeling may represent another phenotypic feature linked to frailty according to the phenotype frailty criteria.

Objectives: Non-ST-segment elevation myocardial infarction (NSTEMI) in the elderly is frequently complicated by multiple comorbidities, which influence clinical outcomes. However, the prognostic significance of atrial fibrillation (AF) in this context remains uncertain. This study aimed to evaluate the impact of AF on short- and long-term mortality in elderly patients (≥65 years) with NSTEMI.

Methods: This cross-sectional observational study included 474 NSTEMI patients aged 65 years and older. Participants were stratified into four groups based on age (65-74 vs. ≥75 years) and the presence or absence of AF. One-month and one-year all-cause mortality were assessed as the primary and secondary endpoints, respectively.

Results: AF was detected in 23 (11.6%) of 199 patients aged 65-74 and in 80 (29.1%) of 275 patients aged ≥75. While one-month mortality did not differ significantly among the four groups (p = 0.514), one-year mortality showed a statistically significant difference (p < 0.001). Univariate analysis revealed that AF was not predictive of one-month mortality. In multivariate Cox regression analysis, AF, reduced creatinine clearance, and left ventricular ejection fraction <50% were identified as independent predictors of one-year mortality.

Conclusion: AF is not associated with short-term mortality in elderly NSTEMI patients; however, it serves as an independent predictor of one-year mortality. These findings highlight the importance of long-term rhythm monitoring and management in this high-risk population.

The pharmacologic management of patent ductus arteriosus (PDA) presents a challenge to clinicians due to the interindividual variability in drug response to available medications. There is evidence that CYP2C9 is associated with the response to PDA treatment; however, no data from the Middle East is available. This study aimed to investigate the association between CYP2C8 and CYP2C9 genetic polymorphisms and response to ibuprofen or indomethacin in neonates with PDA. We conducted a retrospective cohort study of neonates with a gestational age < 32 weeks and birthweight < 1500 g with PDA between 2019 and 2023. Eligible neonates were those diagnosed with PDA and treated with at least one course of ibuprofen or indomethacin. Genotyping was performed to identify four single-nucleotide polymorphisms (SNPs), namely CYP2C8*3 rs10509681, CYP2C9*2 rs1799853, CYP2C9 rs2153628, and CYP2C9*3 rs1057910. Allele frequencies were compared between responders and non-responders, and non-genetic predictors were assessed using logistic regression. A total of 146 infants were identified. Of these, 86 were enrolled. Genetic analysis showed that the heterozygote genotype (TC) for the CYP2C8 gene was the most common (45%), while wild-type alleles were predominant for CYP2C9 variants. No significant differences in allele frequencies were found between responders and non-responders to the treatment (p > 0.05). In a secondary analysis, the need for multiple surfactant doses independently predicted poor response (aOR 0.244, 95% CI 0.086-0.693, p = 0.008), while extremely low birth weight showed a borderline association (aOR 0.281, 95% CI 0.062-1.268, p = 0.099). Carriers of CYP2C8*3 rs10509681, CYP2C9*2 rs1799853, CYP2C9 rs2153628, and CYP2C9*3 rs1057910 were not associated with variations in response to NSAIDs.