Search Results (513)

Background: Dual antiplatelet therapy (DAPT) with a potent P2Y12 inhibitor is recommended for patients with acute coronary syndrome (ACS) following percutaneous coronary intervention (PCI). On-treatment platelet reactivity has been associated with ischemic endpoints and may vary between male and female patients. We, therefore, investigated sex-related differences in on-treatment platelet reactivity in ACS patients receiving ticagrelor or prasugrel. Methods: Maximal platelet aggregation by light-transmission aggregometry (LTA) and platelet surface P-selectin expression in response to arachidonic acid (AA), ADP, collagen, TRAP (a protease-activated receptor [PAR-1] agonist), and AYPGKF (a PAR-4 agonist) were assessed in 80 prasugrel- and 77 ticagrelor-treated patients 3 days after PCI. Results: In the overall study population (n = 157), women were older and had lower serum creatinine, hemoglobin, and hematocrit levels than men (all p < 0.05). Women exhibited higher ADP-inducible platelet aggregation in response to both 10 μM and 5 μM of ADP (both p < 0.05), while no sex-related differences were observed for AA-, TRAP-, collagen-, or AYPGKF-inducible platelet aggregation and agonist-inducible platelet surface P-selectin expression. In prasugrel-treated patients, women had higher ADP-inducible platelet aggregation and P-selectin expression compared with men (both p < 0.05), whereas no sex-related differences were found in ticagrelor-treated patients. In the multivariate linear regression analyses, female sex remained an independent predictor of higher platelet aggregation in response to 5 μM of ADP in prasugrel-treated patients (p < 0.05). High on-treatment residual platelet reactivity (HRPR) in response to AA was detected in four patients, and HRPR ADP was seen in seven patients, with no significant differences between female and male ACS patients (both p > 0.05). Low on-treatment residual platelet reactivity (LRPR) in response to AA was identified in 153 patients and LRPR ADP was present in 80 patients, with a higher prevalence of LRPR ADP in men (p = 0.01). Conclusions: Female ACS patients on prasugrel exhibited higher ADP-inducible platelet aggregation than male patients, while no sex-related differences were observed in patients on ticagrelor. Full article

Background: Antithrombotic therapy plays an important role in acute coronary syndrome (ACS). The combination of anticoagulant and antiplatelet therapy resulted in fewer complications and stronger potency compared to traditional monotherapy. Our net meta-analysis aimed to compare and rank the safety of different treatments used in patients with ACS. Method: We conducted a search for trials in three prominent databases. The main objective of our investigation was to assess hemorrhage. Additional outcomes included mortality, myocardial infarction, stroke, and embolism. We used a frequentist network meta-analysis with a random-effects model to, directly and indirectly, compare safety across different antithrombotic strategies. Result: A total of 30 randomized clinical trials were included in this net meta-analysis with 135,471 ACS patients. In these eight different antithrombotic therapies, SAPT (single-agent platelet inhibitor therapy) showed the lowest risk of bleeding (SUCRA = 0.5%). The highest risk of bleeding was observed in VKA (vitamin K antagonists) + DAPT (dual antiplatelet therapy) (SUCRA = 99.8%). Bleeding among NOAC (non-vitamin K antagonist oral anticoagulants) + DAPT was found to be higher than DAPT (OR = 1.94, 95% CI = 1.42–2.65). NOAC + SAPT significantly reduced the embolism (OR = 1.50, 95% CI = 1.16–1.94) and myocardial infarction (OR = 1.22, 95% CI = 1.08–1.37) events compared with SAPT. In addition, VKA significantly reduced the rate of stroke compared with SAPT (OR = 3.45, 95% CI = 1.17–10.18). However, no significant difference was observed in death events among these eight antithrombotic therapies. Conclusions: We advise against the use of SAPT in ACS due to its elevated risk of embolism, myocardial infarction, and stroke. It is important to mention that the combination of NOAC and SAPT has a lower incidence of myocardial infarction, bleeding and embolism problems. Therefore, the combination of NOAC and SAPT may be the optimal approach to achieve a balance between the risks of bleeding and embolism. This meta-analysis was registered in PROSPERO with the registration number CRD42024542826. Full article

(1) Introduction: Distal coronary emboli occur in up to 15–30.5% of patients undergoing percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI) and are associated with poor myocardial reperfusion in the territory of the infarct-related artery. The objective of this study was to analyze the possible laboratory, clinical and imaging indicators of distal coronary embolism detected with an angiography at the time of PCI with stent implantation for acute coronary syndrome (ACS). (2) Methods: This analysis included 137 patients with ACS. The levels of cardiac enzymes (creatine kinase [CK], muscle–brain fraction of CK, high-sensitivity troponin T [hsTnT]), inflammatory markers (high-sensitivity C-reactive protein, white blood cell counts), sex steroids (total 17β-estradiol, total testosterone, dehydroepiandrosterone sulfate [DHEA-S]), serum lipids and oxidized low-density lipoproteins (oxLDL) were measured and analyzed for their relationship with the incidence of distal coronary embolism at PCI. (3) Results: Slow coronary blood flow was detected in the coronary artery subject to intervention in 9.4% (n = 13) of patients. Triglyceride (TG), high-density lipoprotein (HDL), glucose and serum DHEA-S levels were found to be associated with distal coronary embolization and slow coronary flow at PCI with stenting (DHEA-S: 1.316, OR 1.044–1.659, p = 0.020; TG: 1.130, OR 0.990–1.300, p = 0.072; HDL: 2.326, OR 0.918–5.8977, p = 0.075; glucose: 1.130, OR 0.990–1.300, p = 0.072). In the multivariable model, only DHEA-S after PCI tended to indicate a risk of distal coronary embolism (DHEA-S: p = 0.071; TG: p = 0.339; glucose: p = 0.582; HDL: p = 0.502). (4) Conclusions: Patients with ACS with higher triglyceride levels are at risk of developing slow blood flow after percutaneous intervention with stent implantation. Elevated DHEA-S possibly reflects sympathoadrenal and hypothalamus–pituitary–adrenal hyperactivity associated with ACS and coronary intervention. Full article

Background: Reduced-dose prasugrel is widely used in East Asia for acute coronary syndrome (ACS), but real-world data in diverse Asian populations are limited. This study evaluated its effectiveness and safety in Taiwanese patients. Methods: The PROMISE-TW Registry was a multicenter, retrospective study including 1167 patients with ACS or chronic coronary syndrome (CCS) treated with reduced-dose prasugrel (20 mg loading, 3.75 mg maintenance) across 13 hospitals in Taiwan from 2018 to 2022. The primary endpoint was 1-year major adverse cardiovascular events (MACEs: cardiovascular death, non-fatal myocardial infarction, and non-fatal stroke). Secondary outcomes included composite ischemic events and major bleeding (BARC 3–5). Results: Among enrolled patients (mean age 63.9 years; 81.2% male; 83% ACS), percutaneous coronary intervention was performed in 90.8%. At one year, MACEs occurred in 1.9%, composite ischemic events in 8.2%, and major bleeding in 0.8%. Subgroup analysis identified prior stroke, diabetes, and chronic total occlusion intervention as predictors of bleeding. Male sex, chronic kidney disease, and left circumflex artery intervention predicted higher ischemic risk. Conclusions:Reduced-dose prasugrel provided effective ischemic protection and low bleeding rates in Taiwanese patients, especially those with ACS. These findings support the clinical utility of dose-adjusted prasugrel in East Asian populations and highlight the importance of individualized risk assessment. Full article

Non-ST-segment-elevation acute coronary syndrome (NSTE-ACS) often coexists with multivessel coronary artery disease (MVD), complicating treatment decisions. Current guidelines suggest complete revascularization (CR), yet robust evidence in hemodynamically stable patients remains insufficient. However, the comparative benefit of CR over incomplete revascularization (IR) in reducing ischemic events and improving cardiac function in this population is not well established. The aim of this study was to evaluate the impact of CR on all-cause mortality, cardiac death, and ischemic readmissions at 6 and 12 months, as the composite primary outcome, and to assess left ventricular ejection fraction (LVEF) improvement at discharge and hospital length of stay, as secondary outcomes. A total of 282 hemodynamically stable NSTE-ACS patients with MVD were included, of whom 218 (77.3%) underwent CR and 64 (22.7%) IR. The primary composite outcome occurred in 40.6% of IR patients versus 11.0% in the CR group at 6 months (p < 0.001), and 68.8% vs. 22.0% at 12 months (p < 0.001). CR was associated with significantly lower rates of all-cause and cardiac death, myocardial infarction, and unstable angina. Stroke incidence was similar. Event-free survival favored CR. Multivariable analysis identified CR and baseline LVEF as independent predictors of 12-month outcomes (HR for CR: 7.797; 95% CI: 3.961–15.348; p < 0.001; HR for LVEF: 0.959; CI: 0.926–0.994; p = 0.021). These findings strongly support CR as the preferred therapeutic strategy. Future prospective randomized studies are warranted to confirm the results. Full article

Background and Objectives: In vivo data on healed coronary plaques (HCPs), the hallmark of previous plaque disruption, remains scarce. The study aimed to use optical coherence tomography (OCT) imaging to assess the prevalence, morphological features, and clinical significance of culprit HCPs in patients with acute coronary syndrome (ACS). Materials and Methods: A total of 87 ACS patients (74.3% non-ST-segment elevation ACS) who underwent pre-procedural OCT imaging of the culprit vessel at a single center were retrospectively analyzed. A pilot subgroup of patients with intracoronary thrombi at the culprit site, in various stages of organization and healing, enabled a detailed morphological characterization of HCP despite the absence of histological validation. Three distinct HCP imaging aspects were identified: type I—overlaying fibrous tissue, type II—overlaying lipid tissue, and type III—overlaying calcific tissue. HCP presence was subsequently assessed in the entire population. Clinical correlations included associations with post-stenting outcomes, particularly edge dissections (ED). Results: Culprit HCPs were identified in 78 patients (89.7%): type I—30.8%, type II—51.3%, and type III—17.9%. Regarding the underlying substrate and complication mechanism, type I HCP was associated with pathological intimal thickening (70.8%) and plaque erosion (75%), type II with lipid-rich plaque (80%) and plaque rupture (PR) (82.5%), and type III correlated with calcific plaque (92.9%, p < 0.0001) and both PR and calcified nodule (p < 0.0001). A unique signal-rich ring was observed at the HCP–tissue interface in both type II (77.5%) and type III (78.6%, p < 0.0001). There was a significant correlation between stent ED and HCP presence at landing zones (LZ) (HR 4.14, 95% CI: 1.79–9.55; p < 0.001). Conclusions: OCT analysis of intracoronary organizing fresh thrombi allowed detailed characterization of culprit HCPs and in vivo classification into three imaging types. This approach likely contributed to the high observed detection rate of HCP by enhancing recognition of subtle OCT features. HCP may create mechanical vulnerability if located at the stent LZ. Our improved HCP detection techniques may help optimize stent-related outcomes of OCT-guided procedures by choosing an HCP-free LZ or longer stents. Full article

Background: ESC recommends ticagrelor over clopidogrel for the treatment of acute coronary syndrome (ACS) but the lack of evidence for elderly patients (≥75) and concerns over bleeding has led to significant variability in its use within the UK. Our aim is, therefore, to compare the safety of ticagrelor compared to clopidogrel in real-world elderly patients admitted with ACS and managed either medically or through percutaneous intervention. Methods: Unselected elderly patients (≥75) admitted to Royal Berkshire Hospital with ACS (2013–2015) were identified and followed for 1 year. The primary outcomes were bleeding events (TIMI criteria), all-cause mortality, cardiovascular mortality, ischemic stroke, angina, NSTEMI and STEMI. Results: A total of 288 patients with ACS were discharged with aspirin and either clopidogrel (137) or ticagrelor (151). In total, 152 of these patients underwent invasive angiography and revascularization. The baseline clinical characteristics and crusade bleeding score were similar between the groups receiving ticagrelor or clopidogrel. There were no significant differences in all-cause mortality (8.8% vs. 10.6%), cardiovascular mortality (2.9% vs. 2.0%), ischemic stroke (0.7% vs. 2.0%), angina (6.6% vs. 5.3%) or STEMI (2.2% vs. 1.3%). Patients on clopidogrel, however, had increased events of NSTEMI compared to ticagrelor (8.0% vs. 2.0%, OR 4.481, 95% CI 1.223–16.42) and overall MI (10.2% vs. 3.3%, p = 0.030). No difference was observed in either major (8.8 vs. 8.6%) or minor TIMI bleeding (18.2% vs. 20.5%) and after propensity score matching (minor bleeding p = 0.39, major bleeding p = 0.76). Conclusions: In this real-world analysis, ticagrelor did not increase major or fatal bleeding compared to clopidogrel in elderly patients. In view of the mortality benefit in the large trials, additional cardiovascular benefit of ticagrelor should not be withheld on the basis of age as a perceived risk factor for bleeding in ACS. Full article

Background: The coronavirus disease 2019 (COVID-19), caused by SARS-CoV-2, has had a profound impact on global health, extending beyond pulmonary complications. Cardiovascular involvement in COVID-19 is multifactorial and may be influenced by viral load, inflammatory response, and pre-existing comorbidities. Discussion: Acute complications include myocardial injury, arrhythmias, acute coronary syndromes (ACS), heart failure, Takotsubo cardiomyopathy, myopericarditis, and cardiac arrest. Notably, atrial fibrillation (AF) emerges as a frequent arrhythmic complication, particularly among critically ill patients, and is associated with increased mortality. COVID-19-patients with concomitant ACS present more severe clinical profiles and higher rates of thrombotic events, including stent thrombosis. Cardiac arrest predominantly presents with non-shockable rhythms and is associated with dismal outcomes. COVID-19 also exacerbates heart failure, both by aggravating existing cardiac dysfunction or by precipitating de novo heart failure. Takotsubo cardiomyopathy and myocarditis, although less frequent, have been reported and are often underdiagnosed due to subtle clinical presentations. Right ventricular dysfunction, linked to pulmonary involvement, has emerged as a key prognostic marker. Post-COVID-19 syndrome include persistent cardiac abnormalities such as reduced ventricular function and myocardial inflammation. Cardiac magnetic resonance imaging and strain echocardiography have proven useful in identifying subclinical cardiac involvement. Conclusions: Early recognition and monitoring of cardiovascular complications are crucial for improving outcomes in patients affected by COVID-19. This review summarizes current evidence regarding cardiovascular manifestations associated with COVID-19. Full article

Background/Objectives: Inflammation plays a key role in acute coronary syndromes (ACS). The systemic immune-inflammation index (SII), which integrates immune and inflammatory markers, may serve as a valuable prognostic tool. This study aimed to evaluate the utility of SII as a short-term predictor of mortality and major adverse cardiovascular and cerebral events (MACCE) in ACS patients. Methods: A retrospective analysis was conducted on 964 ACS patients admitted in 2023. SII was calculated from admission hematological parameters. Primary and secondary outcomes were 30-day mortality and MACCE, respectively. Results: SII levels differed significantly across ACS subtypes (p < 0.001), highest in ST-segment elevation myocardial infarction (STEMI) and lowest in unstable angina. SII was markedly higher in deceased patients (2003.79 ± 1601.17) vs. survivors (722.04 ± 837.25; p < 0.001) and remained an independent predictor of mortality (OR = 1.038, p < 0.001). Similarly, SII was elevated in MACCE cases (1717 ± 1611.32) vs. non-MACCE (664.68 ± 713.11; p < 0.001) and remained predictive in multivariate analysis (OR = 1.080, p < 0.001). Predictive accuracy for MACCE was moderate (AUC = 0.762), improved when combined with GRACE 2, especially in specificity (p = 0.07). In STEMI, SII had excellent accuracy (AUC = 0.874), outperforming neutrophil–lymphocyte ratio and C-reactive protein. SII rose at 24 h and declined at 48 h in STEMI, with a slower decline in MACCE patients. Conclusions: SII proved to be a cost-effective biomarker reflecting inflammation, immunity, and thrombosis. Elevated SII predicted short-term MACCE and mortality in ACS, with improved prognostic power when combined with GRACE 2. Persistent elevation may signal ongoing inflammation and increased MACCE risk. Full article

Elevated levels of atherogenic lipoproteins are known to be associated with an increased risk of incident and recurrent cardiovascular events. Knowing that the immediate post-acute coronary syndrome (ACS) period is associated with the maximum risk of recurrent events, the gradual escalation of therapy allows the patient to remain above the targets during the most vulnerable period. In addition, the percentage of lipid-lowering levels for each class of drugs is predictable and has a ceiling. Hence, it is prudent to immediately start with a combination of lipid-lowering drugs following ACS according to the baseline lipid levels. Multiple studies with injectable lipid-lowering agents (PCSK9 inhibitors) such as EVOPACS, PACMAN MI, and HUYGENS MI have shown the feasibility of achieving LDL-C goals by day 28 and beneficial plaque modification in non-infarct-related coronary arteries. Recently, a study from India demonstrated that an upfront triple combination of oral lipid-lowering agents was able to achieve LDL-C goals in a majority of patients in the early post-ACS period. This notion is also supported by a few recent lipid-lowering guidelines advocating for an upfront dual combination of a high-intensity statin and ezetimibe following ACS. Henceforth, the goal should not only be the achievement of lipid targets but also their early achievement. However, the impact of this strategy on long-term cardiovascular outcomes is yet to be ascertained. Full article

Plaque erosion (PE) is now recognized as a common and clinically significant cause of acute coronary syndromes (ACSs), accounting for up to 40% of cases. Unlike plaque rupture (PR), PE involves superficial endothelial loss over an intact fibrous cap and occurs in a low-inflammatory setting, typically affecting younger patients, women, and smokers with fewer traditional risk factors. The growing recognition of PE has been driven by high-resolution intracoronary imaging, particularly optical coherence tomography (OCT), which enables in vivo differentiation from PR. Identifying PE with OCT has opened the door to personalized treatment strategies, as explored in recent trials evaluating the safety of deferring stent implantation in selected cases in favor of intensive medical therapy. Given its unexpectedly high prevalence, PE is now recognized as a common pathophysiological mechanism in ACS, rather than a rare exception. This growing awareness underscores the importance of its accurate identification through OCT in clinical practice. Early recognition and a deeper understanding of PE are essential steps toward the implementation of precision medicine, allowing clinicians to move beyond “one-size-fits-all” models toward “mechanism-based” therapeutic strategies. This narrative review aims to offer an integrated overview of PE, tracing its epidemiology, elucidating the molecular and pathophysiological mechanisms involved, outlining its clinical presentations, and placing particular emphasis on diagnostic strategies with OCT, while also discussing emerging therapeutic approaches and future directions for personalized cardiovascular care. Full article

Background and Objectives: Galectin-3 (Gal-3), a pro-inflammatory cytokine, has been implicated in atherosclerosis and adverse cardiovascular outcomes. While its role in coronary artery disease (CAD) is increasingly recognized, its association with systemic atherosclerosis remains underexplored. Objective: To investigate serum Gal-3 levels in patients with CAD and evaluate correlations between CAD severity and extra-coronary atherosclerotic involvement (carotid, femoral, and radial territories). Materials and Methods: We prospectively enrolled 56 patients with CAD undergoing coronary angiography (42.8% with acute-ACS; 57.2% with chronic coronary syndromes-CCS). Gal-3 levels were measured within 24 h of admission. Atherosclerosis severity was assessed angiographically and through vascular ultrasound of the carotid, femoral, and radial arteries. Patients were stratified by median Gal-3 levels, and clinical follow-up was performed at 1 and 3 months. Results: Gal-3 levels were significantly higher in CAD vs. controls (20.7 vs. 10.1 ng/mL; p < 0.00001) and in ACS vs. CCS (22.18. vs. 17.93 ng/mL; p = 0.019). Gal-3 correlated positively with culprit lesion diameter stenosis (DS) (R = 0.30; p = 0.023) and maximum severity of additional treated lesions (R = 0.62; p = 0.006). Gal-3 also correlated positively with carotid plaque thickness (R = 0.32; p = 0.016), while patients with Gal-3 levels above the median showed increased median values for femoral plaque thickness (32.4 vs. 26.45 mm, p = 0.046). No correlation was found with radial artery calcification. Gal-3 showed moderate discrimination for ACS (AUC = 0.685; cut-off 20.18 ng/mL). On multivariate analysis age, DS, and ACS presentation were independent predictors of Gal-3 above 19.07 ng/mL. Conclusions: Gal-3 levels are elevated in ACS and correlate with atherosclerotic burden, particularly in coronary, carotid, and femoral territories. These findings support Gal-3 as a potential marker of lesion severity and systemic vascular involvement, highlighting its possible role in risk stratification and the monitoring of atherosclerotic disease progression. This study provides integrated insights into the impact of Gal-3 across multiple vascular beds by assessing them concurrently within the same patient cohort. Full article

Spontaneous coronary artery dissection (SCAD) is an increasingly recognized, non-atherosclerotic cause of acute coronary syndrome (ACS), particularly in younger women. This comprehensive review outlines SCAD’s unique pathophysiology, which is linked to underlying arteriopathies like fibromuscular dysplasia, and highlights the critical role of advanced intravascular imaging for accurate diagnosis. A fundamental shift in management is detailed, with evidence favoring a conservative strategy for stable patients due to high rates of spontaneous vessel healing, reserving technically challenging invasive interventions for high-risk cases. Importantly, this review also addresses long-term outcomes, noting significant rates of recurrence and Major Adverse Cardiac Events (MACE), a high prevalence of persistent chest pain, and the central role of beta-blocker therapy in secondary prevention. Ultimately, SCAD requires a departure from standard ACS protocols towards a personalized approach that emphasizes accurate diagnosis, cautious initial management, and vigilant long-term follow-up. Full article

Objectives: This study aimed to evaluate the ability of three-dimensional (3D) speckle tracking echocardiography (STE) to detect acute coronary occlusions in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS) and its potential diagnostic advantage over two-dimensional (2D) STE. Methods: Fifty-six patients with NSTE-ACS (mean age 64 ± 11 years; 80% male) underwent 2D and 3D transthoracic echocardiography prior to coronary angiography. Global longitudinal strain (GLS), global circumferential strain (GCS), and 3D ejection fraction (EF) were analyzed. Acute coronary occlusion was defined as TIMI flow 0–1 in the presumed culprit artery. Results: Acute coronary occlusion was present in 16 patients (29%). Patients with occlusion had significantly more impaired strain compared to those without: 3D GLS (−12.5 ± 2.7% vs. −15.5 ± 2.1%, p < 0.001), 2D GLS (−12.6 ± 2.8% vs. −15.6 ± 2.0%, p < 0.001), 3D GCS (−24.8 ± 4.4% vs. −27.8 ± 4.3%, p = 0.02), and 2D GCS (−18.1 ± 5.5% vs. −22.9 ± 4.7%, p = 0.002). In contrast, 3D EF did not differ significantly between groups (52.5 ± 4.7% vs. 54.7 ± 5.7%, p = 0.16). Receiver operating characteristic analysis showed that 3D and 2D GLS had the highest diagnostic performance (AUCs 0.81 and 0.78), while 3D EF had the lowest (AUC 0.61). Feasibility was lower for 3D STE (86%) than for 2D longitudinal strain (95%, p = 0.03). Conclusions: Both 3D and 2D GLS showed higher diagnostic accuracy than 3D EF in identifying acute coronary occlusion in NSTE-ACS patients. While 3D STE enables simultaneous assessment of multiple parameters, it did not offer incremental diagnostic value over 2D STE and had lower feasibility. Full article

Acute coronary syndrome (ACS) remains the leading cause of mortality in developed countries. Although recent advances have improved our understanding of the pathophysiology of ACS and its primary consequence, myocardial infarction, many questions remain regarding the molecular and cellular changes occurring during and after an infarction. This study aimed to evaluate the expression levels of the zyxin (ZYX) gene in patients with ACS, stable coronary artery disease (stable CAD), and healthy controls. RNA was extracted from PBMCs and analyzed by quantitative real-time PCR (qRT-PCR). Gene expression was measured using TaqMan Gene Expression Assays and the number of ZYX mRNA molecules was quantified based on qRT-PCR kinetics. Kruskal–Wallis was used to compare gene expression levels among the three groups. A significantly higher number of ZYX gene copies was observed in both the ACS and stable CAD groups than in healthy controls (p < 0.0001 and p < 0.001, respectively). A statistically significant difference was also observed between the ACS and stable CAD groups (p = 0.004). The increased expression of zyxin observed in patients with ACS and stable CAD may reflect cellular repair mechanisms activated in response to myocardial injury. Full article