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.
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).
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.
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%).
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.
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).
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.
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).
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.
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.
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.
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 PM2.5, 1.20 (1.06, 1.36) for NO2, and 1.26 (1.11, 1.43) for NOx. 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 PM10, 1.70 (1.27, 2.27) for PM2.5 1.77 (1.32, 2.37) for NO2, and 1.61 (1.21, 2.13) for NOx.
Our findings indicate that long-term combined exposure to multiple air pollutants, including PM2.5, PM10, NO2, and NOx, is associated with an elevated risk of new-onset HF in cancer patients, particularly among individuals with a high genetic predisposition to the disease.
Heart failure (HF) is still an important disease with high mortality rates worldwide. HF treatment is also difficult due to different phenotypes. Diuretic response (DR) is one of the main differences across these subgroups. Novel urinary parameters are used for DR prediction. We sought to determine whether the MELD score could be used as an additional parameter for predicting the DR.
Eighty-one consecutive patients diagnosed with decompensated HF between June and October 2020 were included. The second hour urine sodium (UNa) level after the first intravenous diuretic administration and serum parameters were recorded. All patients underwent a comprehensive echocardiographic examination. MELD score derivatives were tested to assess the DR.
A total of 81 patients (mean age: 66.4 ± 13.5; mean ejection fraction: 29.6 ± 12.7%) were divided into two groups according to UNa. 26 (32%) patients had poor DR. MELD Na score was independently associated with DR (OR = 0.88 [−0.21 to (−0.03)]; p = 0.008). Furthermore, MELD Na score was correlated with urinary sodium (r = −0.354; p = 0.004). Daily furosemide dose was higher (237.9 ± 204.7 vs. 129.3 ± 83.5 mg; p = 0.001) and length of hospital stay was longer (15.6 ± 10.8 vs. 8.5 ± 6.1 days; p < 0.01) in the low UNa group.
The MELD score derivative was associated with DR according to urinary sodium and may be used as an additional parameter to predict the DR.
I read with great interest the correspondence “GLP-1 and Dual GLP-1/GIP Receptor Agonists in Heart Failure With Mildly Reduced or Preserved Ejection Fraction: A Systematic Review and Meta-Analysis” by Ahmed et al. examining the role of GLP-1 receptor agonists (GLP-1 RAs) and dual GLP-1/GIP receptor agonists in patients with heart failure with mildly reduced or preserved ejection fraction (HFmrEF/HFpEF [1]). The authors should be acknowledged for their timely and rigorous synthesis of contemporary randomized data, contributing meaningfully to an important therapeutic gap in HFpEF. Despite these strengths, several limitations inherent to the available evidence deserve emphasis to appropriately contextualize the findings.
First, although all included studies were randomized, many HFpEF outcomes were obtained from post-hoc or secondary analyses of trials mainly designed for obesity, diabetes, or broad cardiovascular risk reduction (e.g., SELECT, FLOW, and EXSCEL). Such analyses are informative but are not well powered for HFpEF-specific endpoints and may be impacted by variations in heart-failure diagnosis and adjudication, thereby limiting causal inference despite randomization [2].
Second, care should be taken when interpreting the lack of a statistically significant effect on cardiovascular or all-cause mortality. The pooled analysis appears underpowered to identify mortality differences, given relatively short follow-up periods and low absolute numbers of deaths in several contributing trials, including SUMMIT. In HFpEF, mortality benefits often require longer follow-up and larger event numbers to become apparent [3, 4].
Third, the generalizability of these findings is limited by the obesity dominant nature of the study populations, with mean body-mass indices consistently above 34 kg/m². Since HFpEF is a heterogeneous syndrome, the observed benefits likely apply mainly to obesity-related or metabolically driven HFpEF. However, extrapolation to lean or non-metabolic HFpEF phenotypes should be undertaken cautiously [5, 6].
In summary, this meta-analysis provides valuable evidence that incretin-based therapies may be a promising adjunctive strategy for selected patients with HFpEF, especially those with obesity and metabolic dysfunction. However, the above limitations highlight the need for prospective, HFpEF-specific randomized trials with broader follow-up and diverse phenotypic representation to clarify the role of these agents across the HFpEF spectrum.
The author received no specific funding for this work.
The author has nothing to report.
The author declares no conflicts of interest.
No new data was created or generated in this work.
Exercise mediates cardiac adaptation in a dose-dependent manner, and each sport has unique demands on the cardiovascular system. Given the long-term effects of key confounding variables such as age, sex, and exercise dose, knowledge gained from one sport cannot be generalized to all sports. Therefore, it is necessary to explore the potential dose-response relationships between different sports and cardiovascular adaptations on a broader time scale, and to explore the regulatory role of key factors such as age and sex.
The China-ACE study will be a prospective longitudinal cohort study involving approximately 500 elite athletes of different sexes, ages, and sports (rowing, canoeing, cycling, triathlon, weightlifting, wrestling, judo, swimming, basketball, badminton, boxing, and beach volleyball) from three provincial sports centers. All athletes will undergo two screenings within 1 year, during which their exercise load and dose will be recorded via quantitative and semi-quantitative methods. The screening will include measuring cardiovascular function, body composition, electrocardiogram, heart rate variability, echocardiography, cardiopulmonary function, circulating biochemical markers, sex hormones, lower limb muscle function, and physical performance.
The China-ACE study will elucidate the potential dose-response relationship between exercise load and cardiovascular adaptation, cardiopulmonary function, skeletal muscle function, and physical performance by continuously tracking the exercise load and exercise dose of athletes in different sports and exploring the potential role of age and sex in these adaptations. This may inform individualized training and cardiovascular prevention for athletes and extend the current understanding of sports cardiology.
Medicaid Expansion (ME) under the Affordable Care Act sought to improve health access though not all states expanded Medicaid. Our goal is to examine whether ME impacts 30-day post-discharge mortality rates for heart failure (HF) hospitalizations.
We constructed a data set incorporating 30-day HF mortality and hospital service area (HSA) characteristics using five sources: (1) Centers for Medicare and Medicaid Services, (2) Medicaid Budget and Expenditure System, (3) US Census Bureau, (4) Dartmouth Atlas of Healthcare, (5) Kaiser Family Foundation. We categorized states as expanding Medicaid by 2014 or not expanding until 2020, excluding five states that expanded between 2014 and 2020. A difference-in-difference (DID) model, adjusted for hospital and HSA factors, was used for analysis.
Among 3839 hospitals, 52% were in ME states. Before 2014, 30-day mortality rates were higher in non-ME state hospitals than in ME state hospitals (11.6% vs. 11.4%; p < 0.001). After 2014, rates increased in non-ME state hospitals (change = 0.11%, 95% CI: 0.04% to 0.18%) but remained unchanged in ME state hospitals (change = 0.01%, 95% CI: –0.07% to 0.08%). The adjusted DID analysis showed a significant disparity in trends between ME and non-ME states (adjusted DID: −0.11%, 95% CI: –0.21% to –0.02%; p = 0.02). A dose-response relationship revealed that each increase of 10,000 new Medicaid enrollees was associated with 0.002% (95% CI: –0.003 to –0.001; p < 0.001) reduced 30-day HF mortality.
Hospitals in ME states maintained stable mortality rates, contrasting with increases in non-ME states, suggesting that improved healthcare access through ME contributed to better outcomes.
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