Frontiers in Cardiovascular Medicine最新文献

Objectives: Recent reports suggest that pulmonary hypertension (PH) is associated with a significantly higher acute mortality after transcatheter aortic valve implantation (TAVI). The aim of this study is to characterize patients undergoing TAVI with preoperative echocardiographically determined severe PH and to investigate acute clinical and long-term outcomes.

Methods: From 2008 to 2021, 3,610 patients with preoperatively documented systolic pulmonary artery pressure (sPAP) underwent TAVI at our institution. The cut off for severe PH was defined as sPAP > 55 mmHg as determined by echocardiography. Severe PH was preoperatively identified in 456 patients. This group was compared to 3,154 patients with sPAP ≤ 55 mmHg. Data were retrospectively analysed according to updated Valve Academic Research Consortium (VARC-3) definitions.

Results: TAVI patients with sPAP > 55 mmHg presented with higher median age (sPAP ≤ 55 mmHg: 81.6 years [interquartile range (IQR): 77.2-85.1] vs. sPAP > 55 mmHg: 82.3 (IQR 77.8-85.8), p = 0.01) and higher prevalence of significant left ventricular dysfunction (LVEF < 35%) (9.7 vs. 15.5%, p < 0.001). Acute outcomes were impaired in patients with severe PH. The detrimental effect of severe PH persisted in Kaplan-Meier analysis one-year after TAVI (mortality rate 20.0 vs. 30.2%, p < 0.001) and in 60-month follow-up (52.0 vs. 65.1%, p < 0.001).

Conclusion: TAVI patients with severe PH represent a high-risk subgroup with unfavourable acute outcomes and increased one-year and long-term mortality. Moreover, the presence of severe PH is associated with increased rates of acute adverse events, including bleeding, need for PPM implantation and renal failure.

Introduction: Mitral regurgitation (MR) is a common valvular disease associated with complications such as pulmonary hypertension, atrial fibrillation, and heart failure. However, its full impact on the cardiovascular system, especially on right heart function, is not yet fully understood. Understanding this relationship is important because the right ventricle (RV) is critical for maintaining cardiovascular function. Dysfunction of the RV, which may be contributed by conditions like MR, is strongly associated with poor clinical outcomes. Despite its importance, comprehensively studying MR's effect on the RV has been challenging due to the complex, interdependent nature of cardiovascular dynamics, limited patient data, and the difficulty in synthesizing disparate information to clarify the left heart-right heart connection.

Methods: The primary goal of this study is to investigate the effects of MR on cardiovascular hemodynamics and RV function by integrating 3D models of the left heart with a closed-loop 0D models of the entire cardiovascular system. We further conduct detailed analyses using patient-specific models to explore how various system modifications impact the RV, providing insights into the nuanced effects of MR on the right heart.

Results and discussion: This analysis provides several clinically relevant insights. First, progressive MR markedly increases RV afterload and predisposes the RV to dysfunction, even when intrinsic RV contractility is preserved or enhanced. Second, MR-specific severity indices and left-heart metrics alone fail to capture the true burden on the right heart; RV impairment can progress despite stable or only modestly changing MR descriptors. Finally, these findings highlight the need to incorporate direct assessment of RV structure and function into the evaluation of MR, as RV vulnerability plays a critical role in determining patient risk and guiding management decisions.

Background: This study aimed to evaluate the early diagnostic value of Serum-Amyloid-A to High-Density-Lipoprotein-Cholesterol Ratio (SHR) for coronary artery disease (CAD) with clinically relevant stenoses and develop a machine learning diagnostic model based on eXtreme Gradient Boosting (XGBoost).

Methods and results: Data from 1,108 CAD patients (with coronary luminal diameter stenosis ≥50% or evidence of functional myocardial ischemia) and 962 controls were retrospectively analyzed. Receiver operating characteristic (ROC) analysis showed SHR (area under the curve (AUC) = 0.769) outperformed C-reactive protein (CRP) (p = 0.006) and Serum amyloid A (SAA) (p < 0.001). Four XGBoost models were constructed, and the best model (CRP + SAA + SHR + 13 other variables) achieved an AUC of 0.876. SHR correlated nonlinearly with age (p < 0.001), and its diagnostic efficacy was higher in younger patients (40 years old, OR = 16.29) than in older adults (80 years old, OR = 4.37). Machine learning models can address the decline in diagnostic capability of SHR in the elderly population.

Conclusion: SHR is a superior composite biomarker for early diagnosis of CAD with clinically relevant stenoses, outperforming CRP and SAA. Machine learning model integrating multiple indicators shows excellent diagnostic performance. Elevated SHR indicates higher CAD risk in younger individuals, providing a new strategy for early screening of CAD with clinically relevant stenoses.

Introduction: Sleep deprivation is known to induce cardiovascular responses. Several studies have shown the beneficial effect of caffeine on neurobehavioral performance during sleep deprivation, but less is known about its influence on the cardiovascular and inflammatory responses associated with sleep deprivation. The aim of this study is to evaluate the impact of acute caffeine intake on (1) peripheral blood pressures, and (2) heart rate, and cutaneous vascular conductance (CVC) and related biomarkers of endothelial activation, during total sleep deprivation (TSD), considering habitual caffeine consumption.

Methods: 41 subjects followed a randomized, placebo-controlled, cross-over study and underwent 2 conditions of TSD (38 h), one with caffeine intake at 09:00 and 14:00 (2.5 mg/kg), and the other with placebo intake.

Results: We confirm that TSD increases systolic and diastolic arterial pressures (p = 0.001 and p = 0.002 for main effects respectively) and heart rate (p = 0.001), and decreases endothelium-dependent and -independent CVC (p = 0.001). Acute caffeine intake inflates the increase in arterial pressures and IL-6 levels, while it does not affect CVC and levels of E-selectin and monocyte chemotaxis protein-1 (MCP-1). Moreover, chronic caffeine consumption had significant main effects on systolic arterial pressure (p = 0.03), heart rate (p = 0.02), IL-6 levels (p = 0.02), and acetylcholine (ACh)-induced CVC (p = 0.02), and interacted with TSD on E-selectin levels and ACh-induced CVC (p = 0.02 respectively).

Conclusion: Acute caffeine intake provokes immuno-inflammatory and cardiovascular responses, and chronic caffeine consumption should be limited to the lowest efficient doses.

Clinical trial registration: https://clinicaltrials.gov/study/NCT03859882, identifier NCT03859882.

Objectives: Percutaneous coronary intervention (PCI) of calcified lesions using stenting may lead to stent malapposition and stent underexpansion. The combination of intravascular lithotripsy (IVL) followed by drug-coated balloon (DCB) treatment may help overcome this limitation. The aim of this single-center, retrospective, registry-based observational study was to assess the efficacy and safety of plaque modification using IVL followed by DCB-only treatment in patients with severely calcified lesions.

Methods: Severely calcified de novo coronary artery lesions were prepared using IVL followed by the application of paclitaxel-coated DCB in 34 consecutive patients; five patients requiring bail out stenting were excluded from the analysis. The cohort included patients both with stable coronary artery disease (53%) and acute coronary syndromes (47%). The mean age of the patients was 75 years and 56% had diabetes. The majority of patients (76%) were at high bleeding risk based on the Academic Research Consortium criteria. The primary endpoint was MACE [major adverse cardiac events, defined as a composite of target lesion revascularization (TLR), myocardial infarction (MI), and cardiovascular (CV) mortality] at 12 months. The secondary endpoints included individual components of MACE at 6 and 12 months and ARC bleeding (BARC) events.

Results: There were no acute vessel closures or perioperative myocardial infarctions. During 12-month follow-up, the primary end point occurred in 15% (n = 5) of the patients, primarily driven by CV death (9%, n = 3) and one type-2 MI (3%). There was only one ischemia driven TLR within 12 months (3%). The rate of Bleeding Academic Research Consortium (BARC) 2-5 and BARC 3-5 bleeding events was 24% and 6% at twelve months, respectively.

Conclusions: PCI using IVL in combination with an application of paclitaxel-DCB strategy was feasible in the treatment of severely calcified coronary artery lesions in this cohort. This novel approach may be particularly advantageous for patents at high risk of bleeding, although further studies are needed to confirm this potential benefit.

Brugada Syndrome (BrS) is a rare but clinically significant inherited arrhythmia disorder characterized by a type 1 ECG pattern and an increased risk of sudden cardiac death (SCD). Since its first description in 1992, BrS has been the subject of intensive investigation, yet risk stratification remains one of its greatest challenges. While survivors of cardiac arrest and patients with documented ventricular fibrillation (VF) are clear candidates for implantable cardioverter-defibrillators (ICDs), predicting risk in asymptomatic or intermediate-risk individuals is less straightforward. Over the past two decades, multiple risk scores have been developed-including the Sieira, Shanghai, BRUGADA-RISK, and PAT-each integrating combinations of clinical, ECG, electrophysiological study (EPS), and genetic data. Performance metrics vary, with C-statistics ranging from 0.70 to 0.82 in derivation cohorts, but external validation has often been limited. Importantly, current ESC and AHA/ACC guidelines only endorse syncope and EPS inducibility as validated predictors, reflecting the cautious stance of expert panels in the face of heterogeneous data. Nonetheless, the emergence of structured risk models has improved our ability to stratify intermediate-risk patients and stimulated further innovation. Looking ahead, opportunities lie in integrating artificial intelligence applied to raw ECG waveforms, wearable technology for dynamic monitoring, advanced cardiac imaging biomarkers, and polygenic risk scores. Multinational collaboration and federated learning will be essential to overcome statistical fragility and ensure global applicability. Ultimately, BrS risk scores should be considered decision-support tools that enrich but do not replace clinical judgment. Shared decision-making remains central, particularly in asymptomatic patients where ICD implantation is not a clear-cut choice.

Objective: This study aimed to identify the independent risk factors for calf muscular vein thrombosis (CMVT) in elderly patients experiencing an acute exacerbation of chronic obstructive pulmonary disease (AECOPD).

Methods: A retrospective study was conducted involving 128 elderly patients (age ≥60 years) with AECOPD. Patients were categorized into CMVT and non-CMVT groups based on lower extremity venous color Doppler ultrasound findings. Clinical characteristics and laboratory parameters were compared between the groups. Statistically significant variables from univariate analysis were incorporated into a multivariate logistic regression analysis to identify independent risk factors. The predictive performance of these factors was evaluated using receiver operating characteristic (ROC) curve analysis.

Results: Multivariate logistic regression identified reduced calf circumference [Odds Ratio (OR) = 0.25, 95% Confidence Interval (CI): 0.1-0.59], elevated red blood cell (RBC) count (OR = 19.85, 95% CI: 1.08-363.96), and elevated D-dimer level (OR = 1.84, 95% CI: 1.13-3.01) as independent risk factors for CMVT. ROC curve analysis demonstrated good predictive performance for these factors, with areas under the curve (AUC) of 0.986 for calf circumference, 0.788 for RBC count, and 0.976 for D-dimer.

Conclusion: Reduced calf circumference, elevated RBC count, and elevated D-dimer level are significant independent risk factors for CMVT in elderly AECOPD patients. Monitoring these indicators could aid clinicians in the early identification and prevention of CMVT in this vulnerable population.

Background: The impact of epicardial adipose tissue (EAT) on the risk of non-obstructive coronary artery disease (CAD) remains unclear. This study aims to investigate the association between EAT and ischemia with non-obstructive coronary arteries (INOCA).

Methods: This study enrolled 281 patients with angina or other symptoms suggestive of myocardial ischemia who underwent single-photon emission computed tomography myocardial perfusion imaging (SPECT-MPI). All patients had confirmed non-obstructive coronary artery disease (stenosis <50%) by either coronary angiography (CAG) or coronary CT angiography (CCTA) within 3 months before or after MPI. Based on MPI results, patients were categorized into ischemic and non-ischemic groups. Epicardial adipose tissue (EAT) density and volume were measured, and relevant clinical parameters were collected for analysis.

Results: The results revealed that 37.72% of the patients had INOCA, and these patients exhibited significantly higher body mass index (BMI) and EAT density. No statistically significant difference in EAT volume was observed between groups. Both EAT density (OR = -1.846, 95% CI: 1.353-2.559, p < 0.05) and volume (OR = -1.703, 95% CI: 1.151-2.551, p < 0.05) were identified as independent risk factors for INOCA. Furthermore, EAT density demonstrated a linear relationship with disease risk. In statin users, the positive association between EAT density and INOCA was attenuated. (β = -0.039, p = 0.046).

Conclusions: EAT density is an independent risk factor for INOCA, with its increase showing a linear association with INOCA risk. Further, statin use was associated with a reduction in this EAT density-related INOCA risk.

Dysglycemia, lipid metabolism, and cardiovascular disease (CVD) progression in type 2 diabetes (T2D) are closely interconnected, yet the non-linear lipid remodeling processes underlying atherogenic dyslipidemia remain insufficiently defined. This study aimed to identify HbA1c thresholds associated with accelerated lipid-driven atherogenesis, quantify the mediating role of the triglyceride-to-HDL cholesterol ratio (TG/HDL-C)-a surrogate of insulin-resistance-related lipid metabolism-and assess the incremental predictive value of the Atherogenic Index of Plasma (AIP) within the clinically ambiguous "glycemic gray zone." A total of 271 adults with T2D not receiving lipid-lowering therapy were retrospectively grouped by HbA1c: good (<7.0%), moderate (7.0%-8.49%), and poor (≥8.5%) control. Atherogenic lipid burden was evaluated using AIP, Castelli indices, TG/HDL-C, non-HDL cholesterol, and remnant cholesterol. Restricted cubic splines were used to explore non-linear HbA1c-lipid relationships; mediation analysis estimated the TG/HDL-C contribution to the HbA1c-AIP pathway; and Net Reclassification Improvement (NRI) tested the added predictive value of AIP over conventional lipid markers. All atherogenic indices worsened with deteriorating glycemia (p < 0.001). Non-linear inflection points were observed at HbA1c 8.0% for TG/HDL-C and 8.5% for AIP (p_non-linearity < 0.01). TG/HDL-C mediated 56.9% of the HbA1c effect on AIP, indicating its central role in linking hyperglycemia to lipid remodeling. Adding AIP improved cardiovascular risk reclassification, particularly in the 8.0%-8.5% transition range (categorical NRI = 0.384; 95% CI: 0.184-0.584). These findings identify 8.0%-8.5% as a metabolically vulnerable HbA1c threshold marked by accelerated atherogenic dyslipidemia. AIP functions as a sensitive lipid-based marker for cardiometabolic risk detection within this gray zone, while TG/HDL-C acts as a key mechanistic mediator, supporting the integration of atherogenic lipid indices into individualized risk assessment and precision lipid management strategies in T2D.

The prevalence of insulin resistance (IR) with associated hyperinsulinemia (HI) is increasing worldwide, as is the prevalence of heart failure with preserved left ventricular ejection fraction (HFpEF). This narrative review aims to explore the epidemiological and pathophysiological relationship between IR/HI and HFpEF, the possible mechanisms by which IR/HI could underlie HFpEF development and worsening, and the actual and future therapeutic implications of this interplay. The prevalence of IR in patients with HF is not negligible, and we will go through the existing literature highlighting this epidemiological association and the longitudinal data supporting a causative link. We will give a brief overview of molecular and physiological mechanisms connecting IR and HFpEF, such as the alteration of vascular homeostasis resulting in endothelial dysfunction and arterial hypertension, myocardial and vascular wall cell growth resulting in microvascular and macrovascular alterations of coronary circulation, and concentric remodeling of the left ventricle resulting in increased stiffness and diastolic dysfunction. We will review the concept of "diabetic cardiomyopathy" as a study model of these correlations. Finally, we will go through existing antidiabetic drugs with a current or potential future role in the treatment of HFpEF and summarize evidence on lifestyle and rehabilitative interventions in the field. Many of the cardiovascular abnormalities caused by IR/HI may be a contributing factor to the development and worsening of HFpEF. Further research is warranted to explore whether early diagnosis and specific treatment of IR/HI in at-risk populations may prevent HFpEF or delay its progression.