Clinical Cardiology最新文献

Background

This study aimed to investigate regional myocardial strain and fibrosis distribution to analyze the apical sparing pattern and the relation with hypertrophy in hypertension.

Methods

This study included clinical and experimental animal investigations. Seventy-three hypertensive patients were divided into two groups: hypertension without left ventricular hypertrophy (HT-NLVH) and hypertension with LVH (HT-LVH). Six 16-week-old male spontaneously hypertensive rats (SHR) and six age-matched male Wistar-Kyoto (WKY) rats were included in this experiment. Echocardiographic measurements were obtained. Myocardial strain indexes, including global longitudinal strain (GLS), the basal, middle, and apical segmental LS (LS-bas, LS-mid, LS-ap), and the proportion of LS-ap/(LS-bas + LS-mid + LS-ap) (P-ap) were measured. The histological collagen volume fraction (CVF) and perivascular collagen area (PVCA) of basal and apical segments (CVF-bas, CVF-ap, PVCA-bas, PVCA-ap) were observed in all rats.

Results

Despite preserved systolic function (FS, LVEF), the HT-NLVH and HT-LVH groups exhibited diastolic impairment (elevated LAVI, E/e’) (all p < 0.05). LS-ap declined only in HT-LVH, while LS-mid and LS-bas worsened from HT-NLVH to HT-LVH, and the HT-LVH group exhibited a significantly elevated P-ap (all p < 0.05). P-ap was associated with LV remodeling indexes and E/e’ (all p < 0.05). Compared with WKY, LS-bas decreased in SHR (p < 0.05). The SHR group demonstrated significantly elevated PVCA-bas, PVCA-ap, and CVF-bas (p < 0.05), while the CVF-ap had no significant difference.

Conclusion

Myocardial dysfunction and fibrosis exhibited regional heterogeneity with predominant basal damage and apical sparing in hypertensive cardiac hypertrophy. This apical-sparing pattern correlated significantly with both diastolic dysfunction and hypertrophic progression, suggesting its potential as a clinically observable hallmark.

Background

C1q/tumor necrosis factor-related protein 12 (CTRP12) plays a protective role in coronary artery disease (CAD) by reducing vascular inflammation. Whether CTRP12 could predict the occurrence of CAD and in-stent restenosis (ISR) occurrence after percutaneous coronary intervention (PCI) treatment remains unknown.

Methods

This retrospective cohort study included patients with CAD who underwent PCI and had serum samples collected at baseline, 24 h, and 72 h post-PCI. The Gensini score was used to assess the severity of coronary artery stenosis. Serum CTRP12 levels were measured using an ELISA kit. Follow-up evaluation of ISR was performed using coronary angiography.

Results

Serum CTRP12 levels were significantly lower in CAD patients than healthy controls (p < 0.001). A negative correlation was found between CTRP12 levels and both the Gensini score (r = −0.37, p < 0.001) and hs-CRP levels (r = −0.43, p < 0.001). Dynamic analysis revealed a significant reduction in CTRP12 levels 24 h post-PCI, with partial recovery observed at 72 h, although levels remained lower than baseline. Patients with ISR consistently demonstrated lower CTRP12 levels than those without ISR (NISR) at all time points. Receiver operating characteristic curve analysis indicated that CTRP12 levels at 24 h post-PCI exhibited the highest predictive accuracy for ISR occurrence.

Conclusion

Serum CTRP12 level may serve as a potential biomarker for diagnosing CAD and predicting ISR occurrence, with significant correlations to disease severity and dynamic changes after PCI.

Background

Patients with acute coronary syndrome (ACS) face a significantly increased risk of cardiovascular events due to vulnerable plaques. However, no clear evidence supports performing preventive percutaneous coronary intervention (PCI) for non-flow-limiting vulnerable plaques. To address this gap, the PASSIVATE-CAP study was designed to investigate the therapeutic potential of drug-coated balloon (DCB) for treating non-flow-limiting vulnerable plaques.

Methods

The PASSIVATE-CAP study is an investigator-initiated, prospective, randomized, multicenter, open-label superiority trial focusing on acute coronary syndrome (ACS) patients with non-flow-limiting vulnerable plaques in non-culprit vessels. In this study, eligible patients will be randomized at a 1:1 ratio into two groups: patients who received guideline-directed medical therapy (GDMT) and patients who received GDMT combined with a drug-coated balloon (DCB). The primary endpoint was the minimal lumen area of the target lesion 1 year after randomization. The secondary endpoints encompass a range of factors, including the proportion of patients with vulnerable plaques in the target vessel, fibrous cap thickness, lipid core arc of the target lesion, minimal lumen area of the target vessel, among others. The study has been registered on Clinicaltrials.gov (Identifier: NCT06416813).

Results: The PASSIVATE-CAP study enrolled its first patient on July 14, 2025, with projected enrollment completion by January 31, 2027. As of December 28, 2025, 6 patients have been enrolled. The anticipated study end date, marking the completion of the follow-up period, is January 31, 2028.

Conclusions

The PASSIVATE-CAP study represents the first prospective, randomized, multicenter, open-label trial designed to explore the therapeutic value of DCB for the treatment of vulnerable plaques within the ACS patient population.

Background

Naples Prognostic Score (NPS), a composite index incorporating inflammatory and nutritional markers, has emerged as a potential prognostic tool in various cardiovascular conditions; however, no meta-analysis has yet pooled the available evidence to comprehensively assess its prognostic utility.

Objectives

To evaluate the association of NPS with clinical outcomes, including all-cause mortality, in-hospital mortality, no-reflow (NR) phenomenon, and left ventricular ejection fraction (LVEF), in acute coronary syndrome (ACS) patients undergoing percutaneous coronary intervention (PCI).

Methods

MEDLINE, Cochrane, and EMBASE databases were searched for studies comparing high and low NPS groups in ACS patients undergoing PCI. Random-effects models were used to pool risk ratios (RR) for binary outcomes and mean differences (MD) for continuous outcomes. Heterogeneity was assessed with I² statistics. Statistical analyses were performed using Review Manager 5.4, and R, version 4.2.2.

Results

We included seven studies comprising 13 268 patients, with 5628 (42.4%) patients in the low NPS group. Low NPS was significantly associated with decreased all-cause mortality (RR: 0.42; 95% CI: 0.32–0.55; I² = 48%) and decreased incidence of NR (RR: 0.60; 95% CI: 0.40–0.88; I² = 83%). Patients with low NPS also had higher LVEF (MD: −2.69%; 95% CI: −3.41 to −1.97; I² = 99%). No significant difference was observed in in-hospital mortality (RR: 0.54; 95% CI: 0.28–1.05; I² = 94%).

Conclusion

In ACS patients undergoing PCI, elevated NPS was associated with worse clinical outcomes. These findings support the use of NPS as a practical, biomarker-based tool for risk stratification in this population.

Objective

To evaluate the incremental value of non-gated chest CT coronary artery calcium score in enhancing GRACE score prediction of major adverse cardiovascular events (MACE) after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS).

Methods

A retrospective cohort study was conducted on 324 ACS patients undergoing PCI and non-gated chest CT. Patients were divided into MACE (n = 100) and non-MACE (n = 224) groups with a median follow-up of 18.7 months. The predictive performance of the GRACE score, Agatston score, and combined clinical composite model was evaluated using receiver operating characteristic (ROC) curves and survival analysis based on optimal cutoff values.

Results

Model 3 (GRACE + CACS) demonstrated AUC values of 0.798 and 0.827 in the training and testing cohorts, respectively, significantly outperforming Model 1 (GRACE) (training AUC = 0.702; testing AUC = 0.758). Model 4, incorporating clinical features, demonstrated optimal predictive performance (training set AUC = 0.806; testing set AUC = 0.857). The AUC differences were statistically significant (p < 0.05). Survival curves revealed the highest MACE incidence (94.4%, p < 0.01) in the high-risk combined Ga1 group (GRACE ≥ 140 and Agatston ≥ 400).

Conclusion

The non-gated chest CT coronary calcification score significantly enhances the predictive value of the GRACE score for major adverse coronary events (MACE) after coronary intervention. When combined with clinical indicators, the predictive power is further improved. Sensitivity analysis confirms the robustness of this finding, providing a reliable tool for clinical risk stratification.

Background

Previous studies have not fully explored the association between air pollutants and heart failure (HF) incidence in cancer participants, nor the role of genetic susceptibility. We aimed to assess air pollutants' impact on HF risk and their joint contribution with genetic susceptibility to incident HF in this group.

Methods

This study utilized data from the UK Biobank and included 50 923 cancer participants. The relationship between air pollutants and the onset of HF was examined using a Cox proportional hazards model. Furthermore, a polygenic risk score was constructed to evaluate the comprehensive impact of air pollutant exposure, genetic susceptibility, and their interactions on the risk of HF among cancer participants.

Results

The research results show that when comparing individuals in the lowest exposure quartile with those in the highest exposure quartile, the multivariate-adjusted HRs were 1.22 (1.07, 1.38) for PM₁₀, 1.16 (1.03, 1.32) for PM_2.5, 1.20 (1.06, 1.36) for NO₂, and 1.26 (1.11, 1.43) for NO_x. For the joint associations, cancer participants with both high genetic risk and elevated air pollutant exposure exhibited the highest risk of HF events. The risk estimates for the incidence of HF were 2.06 (1.52, 2.78) for PM_10, 1.70 (1.27, 2.27) for PM_2.5 1.77 (1.32, 2.37) for NO₂, and 1.61 (1.21, 2.13) for NO_x.

Conclusion

Our findings indicate that long-term combined exposure to multiple air pollutants, including PM_2.5, PM₁₀, NO₂, and NO_x, is associated with an elevated risk of new-onset HF in cancer patients, particularly among individuals with a high genetic predisposition to the disease.