To investigate the effect of dual antiplatelet therapy (DAPT) guided by platelet function testing (PFT) on the prognosis of patients with acute coronary syndrome (ACS) at a high risk for ischemia and bleeding who underwent percutaneous coronary intervention (PCI).
A retrospective analysis was conducted on 1816 patients with ACS and a dual high risk who underwent PCI at a single center from March 2017 to November 2022. Patients were stratified into the guided DAPT group (n = 712) and standard DAPT group (n = 1104) according to whether the patient received PFT. All patients received oral DAPT for a duration of 12 months post-PCI. The deadline for the endpoint was within 12 months of receiving PCI. The primary endpoint was the number of net clinical adverse events (NACEs) that occurred during follow-up, including the composite endpoint of major adverse cardiovascular and cerebrovascular events (MACCEs) and bleeding, as defined by the bleeding academic research consortium (BARC) (type 3 or greater).
Compared with the standard DAPT group, the guided DAPT group exhibited a lower incidence of NACEs (4.8% vs. 8.7%; p = 0.001), MACCEs (3.9% vs. 6.7%; p = 0.017), cardiac death (0.4% vs. 1.5%; p = 0.038), and stroke (0.6% vs. 2.5%; p = 0.005) during follow-up. Cox regression analysis revealed that the incidence of NACEs (hazard ratio (HR): 0.543, 95% confidence interval (CI): 0.363–0.812; p = 0.003), MACCEs (HR: 0.570, 95% CI: 0.364–0.893; p = 0.014), cardiac death (HR: 0.249, 95% CI: 0.072–0.866; p = 0.029), and stroke (HR: 0.174, 95% CI: 0.060–0.501; p = 0.001) in the guided DAPT group was 0.543, 0.570, 0.249, and 0.174 times, respectively, that in the standard DAPT group.
For patients with ACS who are at high risk in the East Asian population, the primary recommendation is to use PFT to guide DAPT within 12 months after PCI, which can reduce the incidence of NACEs, primarily by lowering the rate of MACCEs.
Aortic stenosis (AS) is a prevalent heart valve disease; however, morbidity and mortality are significantly reduced by aortic valve replacement (AVR). The European System for Cardiac Operative Risk Evaluation II (EuroSCORE II) is used to assess perioperative mortality risk in patients with severe AS undergoing AVR. This study aimed to evaluate the prognostic value of EuroSCORE II for long-term all-cause mortality in Chinese patients with moderate-to-severe AS, determine whether AVR affects this prognostic value, and identify the best cut-off value for low-risk EuroSCORE II patients without AVR.
A total of 544 patients with moderate-to-severe AS were divided into four groups based on the associated EuroSCORE II value (cut-off of 4%) and whether the patient had previously undergone AVR. Kaplan–Meier survival analysis, Cox regression, and subgroup analyses were performed to assess the association between EuroSCORE II and all-cause mortality. A receiver operating characteristic (ROC) analysis was used to determine the optimal cut-off value for predicting mortality.
A total of 132 (24.3%) participants reached the endpoint during a median follow-up of 3.45 years. Patients with a EuroSCORE II ≥4% who did not undergo AVR had significantly higher all-cause mortality rates compared to other groups (55.4% vs. 6.5%, 32.7%, and 13.4%; p < 0.001). Kaplan–Meier analysis confirmed these findings (log-rank test, p < 0.001). Cox regression showed a 6.89-fold increased risk in patients without AVR and higher EuroSCORE II values (hazard ratio (HR), 6.891; 95% confidence interval (CI), 3.083–15.401; p < 0.001). The optimal cut-off value for predicting mortality in patients without AVR was 2.23% (area under the curve (AUC), 0.675).
Both EuroSCORE II (cut-off value of 4%) and AVR status were independently associated with the long-term prognosis of patients with moderate-to-severe AS.
NCT06069232, https://clinicaltrials.gov/study/NCT06069232.
A bicuspid aortic valve (BAV) is a common congenital heart disease. The primary treatment for this condition involves the surgical replacement of both the aortic valve and the ascending aorta, typically through the Bentall procedure. Traditionally, the timing of surgery in patients with BAV and aortic dilation is based on the maximum ascending aortic diameter. However, numerous patients who experienced adverse outcomes did not fulfil the established surgical criteria, highlighting the necessity for new predictive factors to guide surgical decisions more effectively. Thus, this study aimed to identify alternative parameters in patients with BAV that could serve as early indicators of surgical intervention and to establish clear threshold values.
A retrospective analysis was conducted among 101 patients diagnosed with BAV at our institution between January 2004 and December 2023 who underwent follow-up computed tomography angiography. Demographic and clinical data were collected, focusing on the influence of ascending aortic volume on adverse outcomes, measured from the aortic annulus to the origin of the brachiocephalic artery.
The average ascending aortic volume, length, and diameter were 99,496.51 mm3, 90.94 mm, and 38.79 mm, respectively. Logistic regression analysis identified that only ascending aortic volume (p = 0.0338) and volume-to-height ratio (p = 0.0331) were significantly associated with adverse outcomes. In a multiple logistic regression model, the volume–height index (VHI) was independently associated with adverse outcomes (odds ratio (OR) 1.0008, 95% confidence interval (CI) 1.00023–1.00182; p = 0.048). Receiver operating characteristic (ROC) analysis determined the optimal cutoff value for the VHI as 66,340.5 mm3/m (area under the curve (AUC) = 0.797, 95% CI 0.676–0.896). The Kaplan–Meier curve showed that the event-free survival rate of patients with a VHI >66,340.5 mm3/m was consistently lower than that of the low VHI group; The difference between the two groups was statistically significant (log rank p < 0.0001).
The VHI is a strong predictor of adverse outcomes in patients with a BAV and can guide surgical intervention decisions.
Calcific aortic valve disease (CAVD) is a progressive condition characterized by inflammation and fibrous calcification remodeling, with aortic valve fibrosis (AVF) representing the associated subclinical phase. Early intervention with oral medication during the AVF stage may prevent and slow the development and progression of CAVD. Previous studies have demonstrated that individuals with diabetes are at an elevated risk of CAVD and also experience a significantly higher incidence of aortic valve stenosis, which rapidly advances from mild to severe stages. Significantly, the adverse effects of glucose fluctuations (GFs) on cardiovascular diseases exceed those associated with persistent hyperglycemia. Nonetheless, the mechanisms through which GFs contribute to AVF, the early stage of CAVD, remain inadequately understood. Consequently, this study aimed to investigate the inflammatory mechanisms underlying AVF induction in response to fluctuations in glucose levels.
Diabetic rat models were established through intraperitoneal injection of streptozotocin (STZ). GFs in these diabetic rats were managed by alternating between a Western diet and periods of fasting. Infliximab was administered to inhibit inflammation mediated by tumor necrosis factor-alpha (TNF-α). For the in vivo study, echocardiographic assessments of the aortic valve and left ventricular function were conducted on the diabetic rats after eight weeks. Aortic valves from various groups of rats were dissected to test fibrosis, extracellular matrix remodeling, and variations in inflammatory factors, which were examined using hematoxylin and eosin (HE) staining, modified Movat–Russell pentachrome staining, and immunohistochemical staining, respectively. For the in vitro study, porcine valvular interstitial cell (VIC) cultures were used to establish GF-induced fibrosis, thereby elucidating the underlying inflammatory mechanisms.
Our study demonstrated that GFs exacerbate AVF and dysfunction in diabetic patients. This is characterized by increased peak blood flow velocity and peak cross-valve gradient of the aortic valve. Furthermore, we observed intensified TNF-α-mediated inflammatory responses, characterized by the upregulation of T lymphocytes and macrophages, as well as activation of the Janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) pathway. Notably, these pathological processes were ameliorated by the administration of infliximab, resulting in the downregulation of fibrotic and inflammatory markers, as well as improved echocardiographic indices. Our research findings indicate that TNF-α-mediated inflammation exacerbates fibrotic aortic valve processes through GFs, which are mediated by the JAK1/STAT3 signaling pathway.
Targeting TNF-α may serve as a potential therapeutic target to mitigate the progression of inflammation-induced aortic valve damage and fibrosis.
Immune checkpoints are critical regulatory molecules in the immune system that maintain self-tolerance by preventing excessive immune activation against healthy tissues while being exploited by malignant cells to promote tumorigenesis and metastasis through immune evasion mechanisms. Immune checkpoint inhibitors (ICIs), represented by programmed cell death protein-1 (PD-1) inhibitors, are a revolutionary class of antitumor therapeutics that have achieved remarkable clinical success over the last decade, with the application of ICIs expanding to a broader spectrum of malignancies. Nonetheless, the administration of ICIs may induce immune dysregulation, potentially leading to the development of multiple immune-related adverse events (irAEs) across various organ systems. Cardiovascular toxicities are a series of relatively rare but severe irAEs that are drawing increasing attention. This review summarizes the latest findings in immune checkpoint signaling pathways and the potential mechanisms underlying the development of various cardiovascular toxicities associated with immunotherapies. Additionally, we also evaluate advances and novel therapeutic targets in the treatment of cardiovascular toxicities.
The procedure of implanting a Micra leadless pacemaker (Medtronic PLC, Dublin, Ireland) via transfemoral venous access carries the risk of vascular complications. Our study examined whether Liu's hemodynamic verification technique, a basic bedside evaluation of flow and pulsatility through the sheath side port before dilator advancement, minimizes vascular complications in Micra implantation.
We conducted a retrospective analysis of 465 consecutive Micra implantations performed at the Department of Cardiology, West China Hospital of Sichuan University, from December 2019 to November 2023. Participants were categorized into two groups: Group A (n = 389), which employed pre-dilation hemodynamic verification with sheath blood flow analysis (Liu's method), and Group B (n = 76), which used standard vascular access. The groups were compared based on demographics, procedural specifics, and vascular complications.
Compared with the standard puncture method, Liu's technique was linked to a much lower incidence of vascular complications (0.5% vs. 3.9%; p < 0.05). No major vascular complications necessitating surgical or endovascular treatment occurred in Group A (0% vs. 2.63%; p < 0.01). The method allowed quick identification of accidental arterial entry and immediate corrective actions without requiring extra specialized tools. No increase in procedure duration or complications related to the Micra device was observed.
In this single-center retrospective study of 465 consecutive Micra implantations, Liu's method for hemodynamic verification significantly reduced the rate of vascular complications and completely prevented major vascular events compared with traditional femoral venipuncture. The technique is straightforward, economical, easy to learn, and could be a viable option when ultrasound guidance is not accessible.
Precise coronary stent implantation is crucial for ostial and partial bifurcation lesions during percutaneous coronary intervention (PCI). Conventional post-dilation coronary stent implantation often causes longitudinal stent deformation (LSD); meanwhile, even a small area of protrusion into the proximal main branch (MB) can lead to severe problems. This study aimed to introduce a novel post-dilation technique, the proximal anchoring technique (PAT), and evaluate the associated feasibility and efficacy in achieving precise stent implantation and preventing LSD.
This bench study was performed in a tapered silicon vessel model, in which 3.5 × 28 mm-sized everolimus-eluting stents (Xience Xpedition™; Abbot, USA) were deployed at a nominal pressure. Post-dilation was conducted using two different strategies: the proximal anchor followed by distal post-dilation group (PAT group) and the conventional post-dilation group (dilation from distal to proximal) (D-P group). After each step, the subsequent changes in stent length were measured by optical coherence tomography (OCT). Additionally, three clinical PCI cases in which PAT and conventional post-dilation were employed are presented.
The longitudinal elongation of stents was significantly increased in the D-P group compared with the PAT group (p < 0.001). The OCT measurements showed that the stents were elongated during every step of the procedure in the D-P group (29.35 ± 0.10 mm vs. 29.65 ± 0.10 mm; p = 0.0054), but only slightly elongated in the first step of the post-dilation in the PAT group (28.73 ± 0.12 mm vs. 28.87 ± 0.12 mm; p = 0.2262).
We present a novel technique, PAT, to assist in more precise coronary stent implantation by preventing LSD for partial ostial and bifurcation lesions during PCI.
Cardiovascular diseases (CVDs) rank among the most prevalent conditions globally, encompassing coronary heart disease, hypertension, cardiomyopathy, and heart failure. The global prevalence of CVD continues to rise despite available therapies such as interventional procedures and pharmacotherapy, which remain associated with high rates of recurrence and mortality. In recent years, with a deepening understanding of the human gut microbiome, researchers have discovered that gut microbiota and their metabolites play a significant role in the development and progression of cardiovascular diseases. Among these, trimethylamine N-oxide (TMAO), a major metabolite of gut microbiota, has garnered extensive attention. Thus, this review leverages a multi-omics perspective to compare the commonalities and differences in TMAO-related mechanisms across various cardiovascular diseases. Moreover, this review aims to construct a TMAO-driven pathogenic network and critically evaluate the translational potential of this metabolite as a disease biomarker and therapeutic target, alongside current challenges.
This study aimed to develop and test an explainable machine learning (ML) predictive model based on lipid-related biomarkers to predict acute coronary syndrome (ACS) in hospitalized patients.
A total of 10,127 consecutive hospitalized patients at three large hospitals were retrospectively studied between 2022 and 2024. ACS incidence was recorded as the primary outcome. Eight ML models were used to calculate the risk of ACS during hospitalization and to distribute patients into low-, intermediate-, and high-risk groups.
All patients were randomly divided into a 70% training set (n = 7088) and a 30% test set (n = 3039). ACS occurred in 1119 (15.8%) and 461 (15.2%) patients, respectively. The Light Gradient Boosting Machine (LightGBM) exhibited the best predictive performance (area under the curve, 0.829) for ACS in the training set. The final model, which included the top 10 features from the LightGBM model, including lipid-related markers and clinical features, achieved a C-index of 0.781 on the test set and demonstrated a significant ability to stratify patients into low-, intermediate-, and high-risk groups.
We constructed a risk-stratification model based on lipid-related biomarkers derived from ML models to predict ACS in hospitalized patients, which could assist in identifying patients with high discriminatory capacity.
The relationship between the albumin-to-alkaline phosphatase ratio (AAPR) and all-cause and cardiovascular and cerebrovascular mortalities, in adults aged 60 years and above, remains unclear. Thus, this study aimed to investigate the relationship between the AAPR and all-cause mortality, as well as cardiovascular and cerebrovascular prognosis, in adults aged at least 60 years.
A total of 13,603 eligible participants were included. Kaplan–Meier curves and log-rank tests were utilized to compare variations in all-cause, cardiovascular, and cerebrovascular mortalities across the AAPR quartiles. Multivariate Cox proportional hazards models and restricted cubic splines (RCS) were applied to examine the associations among the AAPR and all-cause, cardiovascular, and cerebrovascular mortalities.
Cumulative all-cause mortality and cardiovascular and cerebrovascular mortality in the highest AAPR quartile were remarkably lower than in the lowest quartile. A higher AAPR was related to a diminished risk of all-cause mortality [hazard ratio (HR) = 0.64, 95% confidence interval (CI): 0.57–0.71] and cardiovascular and cerebrovascular mortality (HR = 0.73, 95% CI: 0.60–0.90). The AAPR showed a negative linear association with cardiovascular and cerebrovascular mortality (p for nonlinearity = 0.176). In contrast, the relationship between the AAPR and all-cause mortality followed an L-shaped pattern (p for nonlinearity < 0.001).
The AAPR is important in predicting the risks associated with all-cause mortality and cardiovascular and cerebrovascular mortality, providing meaningful insights into mortality risk among the older adult population.
Drug-coated balloons (DCBs) are rapidly gaining prominence, owing to the associated expanding clinical applications and therapeutic potential in interventional cardiology. Moreover, a growing body of evidence from randomized trials, observational studies, and meta-analyses supports the efficacy of DCBs across a broad spectrum of coronary lesions, positioning these devices as a viable, stent-free alternative to conventional strategies. DCBs aim to lower the risks inherent to stent implantation, such as stent thrombosis and in-stent restenosis (ISR), and to enable abbreviated dual antiplatelet therapy in high-bleeding-risk (HBR) patients. Although drug-eluting stents (DESs) remain the current standard in percutaneous coronary intervention, DCBs are emerging as a novel and promising option in diverse clinical settings beyond ISR, including de novo lesions in both small and large vessels, bifurcation disease, patients with a high risk of bleeding, and even acute coronary syndromes. This article aims to provide a comprehensive review of the evolving role, evidence base, and expanding indications of DCB-related therapy beyond ISR.
Heart failure with preserved ejection fraction (HFpEF) is recognized as an aging-related clinical syndrome with high mortality, from which systemic inflammation could represent a primary culprit. Thus, this study aimed to evaluate the association between the lymphocyte-to-monocyte ratio (LMR), a systemic inflammation marker, and clinical outcomes, and to explore the mediation effect of the LMR in the relationship between age and mortality for HFpEF.
Participants in the Real-world Data of Cardiometabolic ProtEcTion trial (RED-CARPET) trial were categorized into tertiles based on the recorded LMRs. We employed Cox regression analyses to explore the relationship between the LMR and mortality, as well as mediation analyses to determine whether the LMR serves as a mediator between aging and mortality.
A total of 1274 inpatients with HFpEF were enrolled between May 2015 and December 2023. After a median follow-up period of 4.9 years, there were 166 recorded deaths, of which 82 were due to cardiovascular causes. In the third model, each one-unit increase in standard deviation (SD) for age was correlated with a 1.98-fold increase in the risk of overall mortality (95% confidence interval (CI), 1.66–2.35) and a 1.73-fold increase in the risk of death due to cardiovascular disease (95% CI, 1.36–2.21). Compared to patients in the first tertile of the LMR, those in the third tertile exhibited a lower risk of death (hazard ratio (HR) 0.42; 95% CI (0.27–0.65)) and cardiovascular death (HR 0.23; 95% CI (0.12–0.46)). Mediation analyses indicated that the LMR partially mediated the relationship between age and cardiovascular mortality in patients with HFpEF, with a mediation proportion of 17.9% (95% CI (7.2%–36%); p < 0.001).
The LMR may serve as a marker for mortality and is implicated in the mediation of age-related cardiovascular death in patients with HFpEF. This study offers a cost-effective predictor for HFpEF and suggests potential mechanisms related to immunosenescence and inflammation-related aging (inflamm-aging).
While the association between estimated glomerular filtration rate (eGFR) and cardiovascular disease has been well established in younger populations, the prognostic significance of this marker in older individuals remains less well defined. Thus, this study aimed to evaluate the predictive value of eGFR in patients aged 80 years or older with acute coronary syndrome (ACS).
We enrolled 551 patients aged ≥80 years hospitalized for ACS, who had the eGFR calculated at admission. The participants were further stratified into three groups by eGFR levels: Low-eGFR group (L-eGFR, eGFR < the 20th percentile), Medium-eGFR group (M-eGFR, the 20th percentile ≤ eGFR < the 80th percentile), and High-eGFR group (H-eGFR, eGFR ≥ the 80th percentile). Major adverse cardiovascular events (MACEs) were recorded during the follow-up period.
During a median 63-month follow-up, the L-eGFR group exhibited a higher cumulative incidence of MACEs, while the H-eGFR group showed a relatively improved prognosis compared with the M-eGFR group. A multivariate Cox regression analysis revealed that reduced eGFR levels remained independently predictive for long-term MACEs. Compared with the M-eGFR group, the L-eGFR group showed a higher risk (hazard ratio (HR) 1.542, 95% confidence interval (CI): 1.104–2.155). The H-eGFR group exhibited a protective effect (HR 0.643, 95% CI: 0.438–0.943).
Reduced eGFR levels were independent predictors for long-term MACEs in older ACS patients. The H-eGFR group had an improved prognosis, suggesting that further exploration of the underlying mechanism linking renal function and prognosis is warranted.
Cacao, the primary raw material for chocolate and certain beverages, is widely cultivated in the Americas and Asia. Furthermore, various components of cacao, including phenolic compounds, have been shown to be effective in preventing numerous diseases. Notably, cacao is particularly effective in preventing cardiovascular diseases (CVDs) by regulating various biomarkers and signaling pathways. The functionality of cacao has been reported in multiple in vitro and in vivo studies and clinical trials, thereby further confirming its efficacy. However, comprehensive reviews on the recently reported preventive effects of cacao on CVDs and the related mechanisms in vitro, in vivo, and in clinical trials remain limited. Thus, this review aimed to provide an overview of the latest research results on the effects of cacao on the prevention of CVDs and on biomarkers associated with these mechanisms. Cacao shows significant potential to prevent and mitigate CVDs, with promising findings that could shape the future of cardiovascular health and functional plant innovation. However, to fully harness the potential of cacao, future research must focus on standardizing bioactive compound content, assessing bioavailability and metabolic pathways, and establishing dose–response relationships across diverse populations.
Notably, most ventricular tachycardia (VT) episodes in patients with VT attributable to structural heart disease are not hemodynamically tolerated. Therefore, techniques for substrate mapping during stable intrinsic or paced rhythm have been developed that eliminate the need to induce VT. Moreover, advances in catheter technology, enabling high-density multi-electrode mapping of abnormal electrograms, have improved the ability of electrophysiologists to identify the substrate responsible for scar-related VT. In addition to the conventional identification of late potentials and local abnormal ventricular activity (LAVA), several substrate imaging approaches have been developed, including the identification of sites of conduction slowing via isochronal late activation mapping and the modification of wavefronts by changing the pacing site. Further, a new near-field algorithm provides a degree of objectivity to the previously subjective annotations of local potential timing. Additionally, changes in the substrate within the scar, specifically the induction of a line of block and subsequent alteration of a LAVA by decremental conduction, can identify functional abnormal ventricular activity that contributes to the development and maintenance of VT and can further improve the accuracy of substrate mapping. Novel cardiac magnetic resonance imaging and computed tomography analyses, facilitated by specialized software, also provide information for non-invasive estimation of the VT isthmus location. Therefore, continued clinical implementation of these techniques and technologies has the potential to improve safety, reduce the complexity, and expand the number of patients who can safely undergo VT ablation.
Cardiovascular-kidney-metabolic (CKM) syndrome represents a progressive disorder characterized by the interplay of cardiovascular pathologies, chronic renal impairment, and metabolic dysregulation. Therefore, this study aimed to examine the relationship between the dietary index for gut microbiota (DI-GM) and mortality outcomes, including both all-cause and cardiovascular-specific mortality, in individuals classified with CKM syndrome stages 0–3.
Our study cohort consisted of 7884 adult participants aged 30–79 years from the National Health and Nutrition Examination Survey (NHANES) conducted between 2007 and 2018. Dietary intake data obtained through 24-hour dietary recalls and food frequency questionnaires were used to calculate the DI-GM scores, incorporating both components beneficial to the microbiota and those with potentially detrimental nutritional effects. The primary and secondary endpoints were all-cause mortality and cardiovascular-related mortality, respectively. The Kaplan–Meier survival analysis, Cox proportional hazards regression models, and restricted cubic spline (RCS) techniques were employed in the statistical analyses.
The participants had a median age of 50 years, with females comprising 52.97% of the cohort. Over a median follow-up period of 77 months, we documented 469 all-cause deaths (4.56%) and 105 cardiovascular fatalities (1.02%). Elevated beneficial scores for the DI-GM demonstrated significant inverse associations with both all-cause (p < 0.001) and cardiovascular mortality (p = 0.017). However, while the total DI-GM scores showed correlation with decreased all-cause mortality (p < 0.001), no significant association emerged for cardiovascular mortality. Following the employment of a comprehensive adjustment, the hazard ratio (HR) for the total DI-GM score and all-cause mortality was 0.90 (95% confidence interval (CI): 0.82–0.98). For the beneficial components, the HR was 0.88 (95% CI: 0.79–0.98) for all-cause mortality and 0.87 (95% CI: 0.77–0.99) for cardiovascular mortality. RCS modeling revealed a U-shaped correlation between the total DI-GM scores and all-cause mortality, which was in contrast to a linear association for the beneficial scores. The systemic inflammation index (SII) accounted for 5.29% and 8.45% of the observed associations between the total and beneficial DI-GM scores and all-cause mortality, respectively.
Elevated DI-GM dietary scores, particularly those emphasizing food components beneficial to the gut microbiota, demonstrate protective associations against both all-cause and cardiovascular mortality in individuals with CKM syndrome in stages 0–3. These protective effects appear partially influenced by systemic inflammatory pathways.
This study aimed to investigate the association between electrocardiogram (ECG) P-wave dispersion (Pd) in sinus rhythm and the risk of new-onset atrial fibrillation (NAF) within one year, to identify high-risk individuals earlier and improve clinical outcomes.
(1) This retrospective nested case–control study included patients diagnosed with NAF at Changzhou First People's Hospital between July 2022 and June 2023. Cases were defined as individuals without a previous atrial fibrillation (AF) diagnosis who developed NAF regardless of symptom status. Controls were matched 1:3 by age and sex from individuals with sinus rhythm during the same period. (2) Using the date of the NAF diagnosis as the index date, then ECGs, echocardiographic data, laboratory tests, and basic clinical characteristics in the sinus rhythm were collected via the electronic medical record system for all subjects within one year post-index date. (3) Differences in ECG parameters, echocardiographic parameters, blood biological indicators, and basic clinical characteristics in the sinus rhythm were compared between the two groups. (4) Conditional logistic regression models were used to evaluate the association between relevant ECG indicators and NAF, with curve fitting performed using generalized additive models (GAMs).
(1) A total of 824 participants were enrolled, including 206 NAF cases and 618 matched controls. (2) A comparison between groups identified significantly higher diastolic blood pressure, glycated hemoglobin A1c, serum creatinine, P-wave duration, Pd, and left atrial diameter in the NAF group than the control group; meanwhile, uric acid, total cholesterol, high-density lipoprotein, and low-density lipoprotein were significantly lower (all p < 0.05). (3) In fully adjusted conditional logistic regression models, increased Pd was independently associated with a higher risk of NAF within one year (odds ratio (OR): 1.149; 95% confidence interval (CI): 1.099–1.202; p < 0.001). Curve fitting demonstrated a positive correlation between Pd and the risk of NAF.
ECG Pd in the sinus rhythm was independently and positively associated with the risk of NAF within one year.
Cardiovascular diseases (CVDs), such as atherosclerosis, myocardial remodeling, myocardial ischemia-reperfusion (I/R) injury, heart failure, and oxidative stress, are among the greatest threats to human health globally. The molecular mechanisms underlying CVDs have not yet been fully elucidated, but progress has been made in research on epigenetics in CVDs. Post-translational modifications (PTMs), which involve the covalent attachment of functional groups to modulate protein structure and function, represent a critical regulatory mechanism. These modifications enhance the functional diversity of the proteome without the need for de novo protein synthesis. Traditional types of PTMs, such as phosphorylation, acetylation, and ubiquitination, are closely associated with the pathogenesis of CVDs. With the application of high-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS), an increasing number of novel acylation modifications have been discovered, including propionylation, butylation, crotonylation, succinylation, lactylation, and isonicotinylation. A deeper understanding of the role of PTMs in CVDs is essential for unraveling their molecular regulatory mechanisms and identifying new biomarkers and therapeutic targets. This review summarizes the mechanisms related to the occurrence and development of CVDs associated with three novel acylation modifications: crotonylation, lactylation, and succinylation.
A paradox persists in contemporary heart failure (HF) care, whereby the therapies most clearly proven to save the most lives are also those most frequently interrupted, often for reasons that are more physiological than pathological. Indeed, during HF medical therapy bradycardia, modest increases in creatinine or potassium levels, mild reductions in blood pressure, and concern regarding hypoglycemia are frequently perceived as dangerous adverse effects of drugs therapy, leading to premature dose reductions or discontinuation. However, when interpreted within their pharmacological and physiological context, these findings more often reflect predictable, dose-related drug effects rather than true toxicity. In the absence of predisposing conditions, such changes are typically modest in magnitude and unlikely to progress to clinically relevant pathological alterations. Recognizing these signals as expected manifestations of effective therapy, rather than harmful events, allows clinicians to maintain evidence-based drugs at target or near-target doses and to fully realize the mortality reduction associated with comprehensive guideline-directed medical therapy (GDMT).
Chemotherapy-induced cardiotoxicity (CIC) is an increasingly recognized complication in cancer survivors, particularly with anthracyclines, human epidermal growth factor receptor 2 (HER2) inhibitors, vascular endothelial growth factor (VEGF) inhibitors, and immune checkpoint inhibitors. CIC may present acutely, chronically, or as a delayed condition, with phenotypes ranging from asymptomatic myocardial dysfunction to heart failure, arrhythmias, and myocarditis. This narrative review aimed to summarize the latest evidence on the pathogenesis of CIC and evaluate traditional and emerging biomarkers for early detection and risk stratification. We comprehensively reviewed the literature related to the pathogenesis and biomarkers of CIC, focusing on studies that examined oxidative stress, DNA damage, mitochondrial dysfunction, inflammation, and immune activation. The five most frequently reported mechanisms in CIC toxicity were oxidative stress, DNA damage, mitochondrial dysfunction, inflammation, and immune activation. Traditional biomarkers, such as cardiac troponin and natriuretic peptides, have been shown to aid in early detection; however, these biomarkers are limited by specificity and timing. Emerging biomarkers, including inflammatory cytokines, fibrosis-related proteins, extracellular vesicles, and non-coding RNAs, demonstrate greater sensitivity and potential for earlier risk stratification. However, study heterogeneity and limited validation across populations hinder clinical translation. Thus, integrating biomarkers with imaging modalities and standardized protocols may enhance personalized surveillance of CIC toxicity. Large prospective studies and standardized frameworks are essential. Hence, a multiparametric approach combining molecular, functional, and computational tools may define future precision monitoring for CIC toxicity.
The controlling nutritional status (CONUT) and allostatic load (AL) indices indicate significant correlations with heart failure (HF). Given that depressive status associated with metabolic dysregulation may influence these associations, this research aimed to explore whether depressive status modulates the associations between these two indices and HF.
Data were analyzed from 4632 participants aged ≥20 years in the National Health and Nutrition Examination Survey (NHANES), 2005–2018. After applying weighting (WTINT2YR) to the included data, samples with missing data and those without weighted processing were excluded. Binary logistic regression analysis was then employed to investigate the relationships between CONUT, AL, and HF. Subgroup analysis was performed with depressive status as a stratifying factor, and a restricted cubic spline (RCS) model was used to investigate the presence of linear or non-linear relationships between the two clinical indices and HF. Receiver operating characteristic (ROC) curves, net reclassification improvement (NRI), and integrated discrimination improvement (IDI) were employed to evaluate the predictive performance of the different models for HF.
Both CONUT and AL were positively correlated with HF in Model 1 (CONUT: odds ratio (OR) = 1.43, 95% confidence interval (CI): 1.25–1.63, p < 0.001; AL: OR = 1.23, 95% CI: 1.14–1.32, p < 0.001) and Model 2 (CONUT: OR = 1.29, 95% CI: 1.12–1.48, p < 0.001; AL: OR = 1.14, 95% CI: 1.05–1.24, p = 0.002). Depressive status was shown to moderate the positive association between CONUT and HF (p for interaction = 0.035). AL was associated with HF in the depressive subgroup (area under the curve (AUC) = 0.6048, 95% CI: 0.5162–0.6934), indicating limited predictive performance of the model. The NRI and IDI values revealed no significant difference in the predictive performance of CONUT and AL in Model 4.
The CONUT and AL indices demonstrated positive associations with HF in the general population. Depressive status is a moderating factor that attenuates the association between CONUT and HF. Meanwhile, CONUT and AL are not effective predictors of HF risk under conditions of depressive status. Therefore, screening for depressive status in individuals with high CONUT and AL indices is important for predicting HF.
The role of euthyroid hormone levels in clinical outcomes after drug-coated balloon (DCB) angioplasty in patients with coronary heart disease (CHD) remains unclear. Thus, this study aimed to explore the relationship between thyroid function and the risk of restenosis at one year, as well as the prognosis over five years in euthyroid patients with CHD following DCB angioplasty.
This prospective study evaluated 189 euthyroid CHD patients who underwent successful DCB angioplasty. Coronary angiographic follow-up was performed 9–12 months post-procedure to assess the status of target lesions, with restenosis defined as ≥50% reduction in luminal diameter. All patients underwent five-year clinical follow-ups, during which major adverse cardiovascular events (MACEs) were recorded.
Following angiographic follow-ups, patients were categorized into two groups: those with restenosis (n = 66) and those without (n = 123). At baseline and during the follow-up, the restenosis group demonstrated significantly higher levels of thyroid-stimulating hormone (TSH), lymphocytes, hemoglobin A1c (HbA1c), lipoprotein(a), and platelet count, along with lower free triiodothyronine (FT3) levels. Multivariable logistic regression analysis revealed that the TSH levels both at the baseline (odds ratio (OR) 1.607, 95% confidence interval (CI) 1.238–2.085, p < 0.001) and angiographic follow-up (OR 2.970, 95% CI 2.000–4.411, p < 0.001) were independently associated with an increased risk of post-DCB restenosis. Furthermore, patients in the high TSH tertile had a 90% increased risk of MACEs during the 5-year follow-up period (hazard ratio (HR) 1.922, 95% CI 1.343–2.750, p < 0.001) compared with those in the low TSH tertile.
A high-normal TSH level within the euthyroid range was strongly associated with an increased 1-year restenosis risk and decreased 5-year MACE-free survival following DCB angioplasty in CHD patients.
Managing ischemic cardiomyopathy-related ventricular tachycardia (VT) remains clinically challenging since no definitive consensus exists regarding the optimal therapeutic approach. Therefore, this study aimed to assess the safety and efficacy of catheter ablation for VT in patients with ischemic cardiomyopathy.
We systematically searched the PubMed, EMBASE, and Cochrane Library databases to identify pertinent clinical trials. We selected the relative risk (RR) and mean difference (MD) as the effect measures, which were calculated using Review Manager software. Additionally, we used trial sequential analysis to assess each outcome.
Our study included six randomized controlled trials with 1064 patients. Catheter ablation was found to reduce the risk of the composite endpoint (RR 0.83, 95% confidence interval (CI) 0.74–0.94; p = 0.002), cardiac hospitalizations (RR 0.82, 95% CI 0.71–0.95; p = 0.007), and adverse events (RR 0.75, 95% CI 0.62–0.91; p = 0.003). Additionally, no significant differences were observed between the two groups regarding VT recurrence (RR 0.94, 95% CI 0.83–1.06; p = 0.33), appropriate implantable cardioverter-defibrillator (ICD) shocks (RR 0.85, 95% CI 0.72–1.01; p = 0.06), or all-cause mortality (RR 0.93, 95% CI 0.73–1.18; p = 0.53).
Catheter ablation reduced the incidence of composite endpoints, cardiac hospitalizations, and adverse events related to VT in patients with ischemic cardiomyopathy. However, no statistically significant differences were found between the two groups for VT recurrence, appropriate ICD shocks, and all-cause mortality.
Takotsubo syndrome (TS) is an acute cardiac disease entity characterized by a reversible regional, usually circumferential, left ventricular wall motion abnormality in patients presenting with a clinical picture resembling that of acute coronary syndrome with non-obstructive coronary arteries. Overwhelming evidence supports the involvement of sympathetic nervous system hyperactivation in the pathogenesis of TS. Therefore, the diagnostic pathogenic term of autonomic neurocardiogenic (ANCA) syndrome has also been introduced. An association between TS or ANCA syndrome and “myocarditis” has been reported. The definitive histopathological diagnosis of acute “myocarditis” is based on myocardial infiltration with mainly mononuclear cells and signs of non-ischemic myocyte necrosis with or without fibrosis. The radiological diagnosis of myocarditis is based on the cardiac magnetic resonance (CMR) imaging findings of hyperemia, myocardial oedema, and non-ischemic myocardial necrosis/fibrosis. These endomyocardial biopsy and CMR imaging findings may also be seen in TS or ANCA syndrome and have been interpreted as true “myocarditis”. However, histopathological changes in TS or ANCA syndrome begin with hypercontraction of sarcomeres, and myocardial cells may die in a tonic state if hypercontraction is severe and persistent. This myocardial cell necrosis elicits mononuclear cell infiltration, followed by fibrosis and scarring. Mononuclear cell infiltration occurs as a response or secondary process following the development of myocardial cell necrosis. Regrettably, these histopathological “secondary myocarditis-like changes” and the consequent CMR imaging findings have been, and at times remain, misdiagnosed as true “myocarditis” for many decades. These misinterpretations have been critically reviewed, analyzed, and illustrated with revealing images and with a novel conclusion.
Distal radial access (DRA) has emerged as a preferred approach in cardiac and peripheral vascular catheterization, offering distinct advantages over traditional access methods. However, DRA is inherently more challenging due to the smaller diameter, sharper angulation, and greater anatomical variability of the vessels, which collectively increase the risk of puncture failure and the need for crossover to alternative vascular access. Thus, ultrasound guidance has become increasingly important. Unlike the conventional transradial approach, where ultrasound guidance remains optional, the use of ultrasound guidance in DRA could offer additional benefits, including potentially improved success rates and a reduced risk of damage to surrounding anatomical structures. This review highlights the essential role of vascular ultrasound in DRA and presents a detailed, step-by-step guide that integrates sonographic and anatomical techniques. Therefore, by promoting technical precision and ensuring safer vascular access, this approach aims to optimize the success and safety of catheterization procedures and foster the widespread adoption of DRA in clinical practice.
This study aimed to review the unique contribution of the Seven Countries Study (SCS) of cardiovascular diseases to the possible non-heterogeneity in multivariate coefficients of serum cholesterol in predicting coronary heart disease (CHD) mortality across different populations. This study reviewed five published analyses from the SCS, which together encompassed 16 cohorts of middle-aged men from eight nations across seven countries in the USA, northern and southern Europe, and Japan. In total, these analyses included 12,763 participants and follow-up periods ranging from 25 to 60 years after the baseline examination. Serum cholesterol was measured using uniform, standardized procedures that differed from those reported in the literature. Marked differences in mortality rates were observed, with higher rates in the USA and northern Europe and lower rates in the other regions. A systematic comparison of serum cholesterol coefficients did not reveal significant heterogeneity across cohort combinations or follow-up durations of 25, 40, 50, and 60 years for CHD mortality. In all cases, coefficients were adjusted for three additional risk factors: age, cigarette smoking, and systolic blood pressure. Variations in CHD mortality rates across populations were explained by differences in serum cholesterol levels. In contrast, the magnitudes of serum cholesterol coefficients were relatively similar across groups, although not necessarily homogeneous. These findings support the idea that predictive models of CHD mortality developed for a specific population can also be applied to other populations, since the expectation, at least for serum cholesterol, is to obtain similar relative risk estimates, not absolute risk, which aligns with the limited evidence that is available in the current literature.
Cardiovascular–kidney–metabolic (CKM) syndrome embodies the interconnection between cardiovascular, renal, and metabolic disorders. Anthropometric indices reflect distinct aspects of obesity and may aid in stratifying the severity of CKM syndrome and predicting mortality. Thus, this study aimed to assess and compare the relationships between multiple obesity-related measures and advanced CKM stages, as well as the risk of mortality.
Data included in this analysis were from the National Health and Nutrition Examination Survey (NHANES). Participants were categorized into quartiles (Q1–Q4) based on each anthropometric index. We estimated the associations with all-cause, cardiovascular, and non-cardiovascular mortality outcomes using Cox proportional hazards models, and evaluated the odds of an advanced CKM stage (stages 3/4) using logistic regression. Possible non-linear exposure–outcome patterns were further investigated through restricted cubic spline modelling. Then, to compare the predictive performance of the indices, we calculated the area under the receiver operating characteristic curve (AUC).
We included 28,911 adults from the NHANES (1999–2018) (median age (interquartile range (IQR)) 55.0 (40.0–67.0) years, 52.5% male), comprising 21,789 in CKM stages 1–2 and 7122 in stages 3–4. The anthropometric indices varied significantly across CKM stages (p < 0.001), with body mass index, waist circumference, Weight-adjusted Waist Index (WWI), and relative fat mass increasing with disease severity. In stages 1–2, the highest quartile (Q4) of A Body Shape Index (ABSI), WWI, waist-to-height ratio (WHtR), and Conicity Index (C-index) was associated with higher all-cause and cardiovascular mortalities, often following U-shaped or J-shaped non-linear patterns. In stages 3–4, predictive strength diminished, with only the ABSI and WWI showing consistent associations with mortality. For CKM progression, the ABSI (AUC = 0.73), WWI (AUC = 0.70), and C-index (AUC = 0.69) demonstrated the best discrimination.
This study shows that several anthropometric indices, particularly the ABSI, WWI, WHtR, and C-index, are strongly associated with advanced CKM stage and increased mortality risk. These associations were stronger for central adiposity measures than for general adiposity, suggesting the potential relevance of central fat distribution and supporting the possible role of anthropometric indices in early risk stratification and targeted intervention in CKM syndrome.
Heart failure is a significant complication following cardiac surgery. While sodium-glucose co-transporter-2 (SGLT2) inhibitors show established benefits in chronic heart failure, their specific role in the perioperative setting remains poorly defined. This review aims to consolidate the current evidence on the beneficial effects and underlying mechanisms of canagliflozin in managing heart failure associated with cardiac surgery. A narrative review of relevant preclinical animal studies and clinical trials was conducted to integrate and summarize the existing data. The evidence demonstrates that canagliflozin confers cardiovascular protection through multifaceted mechanisms, including improved metabolic regulation, favorable hemodynamic effects, and potent anti-inflammatory and anti-fibrotic actions. These mechanisms are highly relevant to mitigating key pathophysiological insults in the perioperative period. While current clinical data are limited to observational studies, they suggest promising benefits for canagliflozin in reducing postoperative cardiovascular complications. Canagliflozin shows considerable potential as a therapeutic agent for patients with heart failure related to cardiac surgery. However, definitive evidence from large-scale, multicenter randomized controlled trials is warranted to confirm its efficacy and safety, and to optimize perioperative management strategies.
Coronary microvascular dysfunction (CMD) is a key driver of ischemia and prognosis across several non-ischemic cardiomyopathies. This review summarizes the main tools for diagnosing microvascular dysfunction and available evidence on CMD incidence and the prognostic role in patients with cardiomyopathies. In dilated cardiomyopathy, CMD is associated with reduced myocardial blood flow, greater fibrosis, adverse remodeling, and worse outcomes. In hypertrophic cardiomyopathy, CMD is highly prevalent and multifactorial (arteriolar remodeling, reduced capillary density, extravascular compression, diastolic dysfunction, and/or left ventricular (LV) outflow obstruction), correlating with fibrosis, heart failure, and arrhythmias/sudden death. In Takotsubo syndrome, CMD appears acute and reversible, with microvascular spasms as a predominant mechanism and plausible pathophysiologic basis of the event. In arrhythmogenic right ventricular cardiomyopathy, preliminary data show a blunted hyperemic response and autonomic abnormalities that may impair microvascular vasodilation. In infiltrative and storage diseases (amyloidosis and Anderson–Fabry disease), CMD is often early, preceding hypertrophy/fibrosis, and contributes to symptoms, contractile dysfunction, and adverse outcomes; in sarcoidosis, microvascular inflammation reduces coronary flow reserve (CFR) and is associated with events. Targeted therapies remain limited; optimization of risk factors and drugs that modulate endothelial/metabolic function (statins, angiotensin converting enzyme (ACE) inhibitors, vasodilating β-blockers, calcium channel blockers, sodium glucose cotransporter 2 (SGLT2) inhibitors) yielded variable signals; device-based and nonpharmacologic strategies are under investigation. In conclusion, integrating microcirculatory assessment improves risk stratification and may furnish future therapeutic targets across cardiomyopathies.
Statins are the cornerstone of lipid-lowering therapy and exert significant pleiotropic effects, including antioxidant and anti-inflammatory actions, which contribute to statin-mediated cardiovascular benefits. A key mechanism underlying these effects is the indirect activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor. This review critically assesses the molecular pathways through which statins modulate Nrf2 signaling, primarily through the PI3K/Akt and ERK pathways, which results in the nuclear translocation of Nrf2 and the transactivation of a battery of cytoprotective genes (e.g., heme oxygenase-1 (HO-1), Nicotinamide Adenine Dinucleotide (Phosphate) (reduced) (NAD(P)H) quinone oxidoreductase-1 (NQO1), catalytic subunit of glutamate–cysteine (GCLC)). This review synthesized evidence on the mechanism through which Nrf2 modulation stabilizes atherosclerotic plaques by mitigating oxidative stress and inflammation within the vascular wall. Furthermore, we explore the cell-type-specific effects of these findings within the complex plaque microenvironment and discuss any unresolved questions, including the therapeutic potential and pharmacokinetic challenges of combining statins with direct Nrf2 activators. Thus, by extending beyond a descriptive summary, this review provides a mechanistic integration of the statin–Nrf2 axis and identifies key frontiers for future research, emphasizing the need to harness these pleiotropic effects for improved cardiovascular outcomes.
The HAVOC score is an emerging tool for estimating the risk of atrial fibrillation (AF), which has attracted growing interest. However, the use of the HAVOC score to predict in-hospital new-onset AF (NOAF) among patients with ST-segment elevation myocardial infarction (STEMI) remains unclear. Therefore, this study aimed to examine whether the HAVOC score is associated with NOAF during the index hospitalization following primary percutaneous coronary intervention (PCI) in patients with a STEMI.
We studied a consecutive cohort of patients presenting with STEMI from January 2023 to March 2025. After primary PCI, each participant underwent continuous electrocardiogram monitoring for at least 72 hours. The HAVOC score was calculated based on hypertension, age ≥75 years, valvular heart disease, peripheral vascular disease, obesity, and heart failure.
In total, 725 patients were analyzed, with a mean age of 63.37 ± 13.16 years; of whom 72.97% were male. During the hospital stay, 70 patients (9.66%) experienced NOAF. Multivariate logistic regression analysis showed that the HAVOC score (odds ratio (OR) = 1.42, 95% confidence interval (CI): 1.28–1.59) was independently associated with NOAF. Restricted cubic spline (RCS) analysis revealed a linear dose–response relationship between the HAVOC score and NOAF (p for overall <0.001). Integrating left ventricular ejection fraction (LVEF) and the presence of left anterior descending artery stenosis enhanced the discriminatory ability of the HAVOC score for identifying NOAF (net reclassification index [NRI] = 0.353, 95% CI: 0.114–0.592; p = 0.004) and improved integrated discrimination (0.024, 95% CI: 0.006–0.041; p = 0.008).
Higher HAVOC scores were independently linked to the occurrence of in-hospital NOAF among STEMI patients following PCI. NOAF risk increased with the HAVOC score, consistent with a linear dose–response across the score spectrum.
Lipoprotein(a) [Lp(a)] represents one of cardiovascular medicine's most profound implementation gaps: a genetically determined risk factor affecting 1.5 billion people worldwide, yet historically underutilized in clinical practice despite overwhelming evidence of its importance. This review examines the transformation of Lp(a) from an untreatable genetic burden to a promising therapeutic target through four interconnected perspectives. First, we document the implementation gap, where, despite affecting 20% of the global population, screening remains below 1%. The evolution from selective screening (2018 American College of Cardiology/American Heart Association (ACC/AHA)) to universal measurement (2024 National Lipid Association (NLA) Class I recommendation) reflects growing recognition, yet persistent barriers, including reimbursement challenges, provider knowledge gaps, and laboratory standardization issues, perpetuate underutilization. Second, we synthesize evidence establishing Lp(a)'s dual nature as both a biomarker and a causal factor. Observational studies demonstrate markedly increased cardiovascular risk with elevated Lp(a), while Mendelian randomization confirms causal relationships with coronary heart disease, large-artery stroke, peripheral artery disease, and aortic stenosis, with differential effects on stroke subtypes and non-atherosclerotic outcomes. Third, we examine the transformation from genetic determinism to pharmacological tractability. Despite 70–90% heritability, novel RNA-targeted therapies achieve unprecedented 80–95% reductions, with phase 3 cardiovascular outcome trials (completing 2026–2029) poised to determine whether dramatic Lp(a) lowering translates to clinical benefit. Finally, we provide a practical management algorithm bridging current evidence-based risk stratification with emerging therapies, stratifying patients by Lp(a) levels with corresponding interventions. The Lp(a) story exemplifies how genetic insights and technological innovation can transform immutable disease aspects into treatable conditions, offering a paradigm for precision cardiovascular medicine while highlighting the urgent need to close the gap between scientific knowledge and clinical implementation.
The circumflex (Cx) coronary artery is more vulnerable to injury than other coronary arteries during procedures such as radiofrequency ablation, left atrial appendage closure, mitral valve repair, and coronary sinus-based mitral valve intervention. Furthermore, a lower success rate was also observed in the Cx artery during chronic occlusion recanalization. Additionally, injury to the great cardiac vein during Cx artery interventions can occur due to the highly variable and often unpredictable relationship between the great cardiac vein and the Cx artery, which occurs in approximately 30% of cases. Imaging information on the Cx artery and the associated relationship with surrounding cardiac structures is crucial for understanding spatial orientation. This knowledge aids preventive measures, accurate prediction, prompt recognition, and understanding of injury mechanisms, thereby facilitating appropriate therapeutic interventions. We present a comprehensive literature review of the clinical implications, complexities, and challenges associated with the Cx artery, which could help in management strategies and improve outcomes.
Type 2 diabetes mellitus (T2DM) is a complex metabolic disorder that is associated with a markedly increased risk of coronary artery disease (CAD) and cardiovascular (CV) mortality compared with the general population. Prediabetes, a heterogeneous intermediate glycemic state defined by impaired fasting glucose (IFG) and/or impaired glucose tolerance (IGT), and/or glycated hemoglobin (HbA1c) levels between 5.7% and 6.4%, is likewise associated with a significantly higher CV risk than normoglycemia. Over the past decade, both overall CAD burden and specific plaque morphologic features have been established as robust predictors of future adverse CV events using invasive and non-invasive coronary imaging modalities. More recently, growing evidence has highlighted the influence of glycemic abnormalities on the extent, progression, and phenotype of CAD, underscoring the interplay between metabolic dysfunction and atherosclerotic vulnerability. Therefore, this review aims to (i) elucidate the pathophysiological mechanisms linking T2DM and prediabetes with atherogenesis, (ii) summarize findings from coronary imaging studies in these populations, and (iii) evaluate therapeutic strategies designed to promote plaque stabilization and regression.
Significant tricuspid regurgitation (TR) is increasingly recognized as a major determinant of morbidity and mortality, yet the clinical impact of significant TR has long been underestimated. Assessment of right ventricular (RV) systolic function is central to understanding and managing TR and represents the principal determinant of symptoms, therapeutic response, and long-term outcomes. The unique sensitivity of the RV to alterations in preload and afterload leads to maladaptive remodeling, making accurate functional assessment essential for risk stratification and for optimizing the timing and type of intervention, especially given the expanding range of available surgical and transcatheter treatment options. Echocardiography remains the primary imaging modality, providing qualitative and quantitative evaluations of RV function through parameters such as tricuspid annular plane systolic excursion (TAPSE), RV fractional area change (RVFAC), and tissue Doppler systolic velocity (S′). Advances in speckle-tracking echocardiography for RV free-wall longitudinal strain and in three-dimensional imaging have improved accuracy; however, all echocardiographic measures remain limited by the complex geometry of the RV. When feasible and available, cardiac magnetic resonance (CMR) imaging serves as the reference standard for precise assessment of RV volumetric and functional parameters. Impaired RV systolic function, both before and after intervention, irrespective of the imaging parameter used for the assessment, consistently predicts adverse outcomes in patients with severe TR, including heart failure progression, reduced exercise tolerance, and decreased survival. Therefore, early recognition and quantification of RV dysfunction are crucial to enable timely therapy, as interventions before the development of advanced RV impairment provide symptomatic and survival benefits. This review summarizes the pathophysiology, quantitative thresholds, and prognostic significance of RV function assessment, emphasizing the pivotal role this evaluation plays in the contemporary management of significant TR.