Search Results (73)

Residual inflammatory risk after acute coronary syndromes (ACSs) remains a critical contributor to atherosclerosis progression and plaque destabilization. Inflammatory biomarkers such as interleukin-1 receptor antagonist (IL-1ra), resistin, and C-reactive protein (CRP) may provide additional insights into coronary lesion complexity and vulnerability. The main aim of the study was to evaluate the association of interleukin-1 receptor antagonist (IL-1ra), resistin, and C-reactive protein (CRP) with coronary disease extent; functional significance of non-culprit lesions, assessed by fractional flow reserve (FFR); and plaque vulnerability, assessed by optical coherence tomography (OCT) in patients with acute coronary syndrome (ACS). This prospective study enrolled 93 ACS patients undergoing invasive coronary assessment for an ACS. Inflammatory biomarkers were measured at admission and 6 months post-event. Patients were stratified post hoc into tertiles by biomarker distribution. SYNTAX score, FFR, and OCT-defined thin-cap fibroatheroma (TCFA) were used to characterize lesion burden and morphology. Multivariate logistic regression was performed adjusting for conventional cardiovascular risk factors and ACS type. Higher tertiles of IL-1ra, resistin, and CRP were significantly associated with increased SYNTAX score (p < 0.05), FFR < 0.80 (68% in the highest tertile), and presence of TCFA (62% vs. 20%, p < 0.01). All biomarkers correlated with coronary disease severity. In multivariate logistic models, IL-1ra (OR 1.23 per 100 pg/mL, p = 0.03), resistin (OR 2.35 per 1 ng/mL, p = 0.001), and CRP (OR 1.11 per 0.001 ng/mL, p = 0.006) independently predicted high-risk coronary profiles. IL-1ra, resistin, and CRP are independently associated with lesion complexity, functional significance, and vulnerability in ACS. Inflammatory biomarker profiling may provide complementary anatomical and physiological assessment in future ACS risk stratification strategies. Full article

Background: The STEMI/NSTEMI classification guides management and quality metrics for acute myocardial infarction (AMI). We examined whether the final cath-lab diagnosis of STEMI versus NSTEMI correlates more closely with door-to-balloon (D2B) time than with either ST-segment elevation (STE) on pre-angiogram ECG or a culprit lesion with TIMI 0-1 flow. Methods: This retrospective study analyzed 410 patients with AMI from the DOMI-ARIGATO database who underwent coronary angiography. For each patient, we recorded FDx coded by the interventional cardiologist, D2B < 120 min versus > 120 min, STE criteria (Fourth Universal Definition), and angiographic TIMI 0-1 culprit. Predictors of FDx-STE discordance were evaluated with multivariable logistic regression. Results: Among 410 angiographed AMI patients (mean age 63 ± 13; 71% male), 165 (40.2%) received an FDx-STEMI and 245 (59.8%) an FDx-NSTEMI. D2B time showed 94% agreement with FDx (160/165 FDx-STEMI treated < 120 min; 225/245 FDx-NSTEMI treated > 120 min), exceeding concordance for STE (82%; p < 0.001) and TIMI 0-1 flow (75%; p < 0.001). FDx and STE diverged in 75 patients (18%): 60 rapidly treated STE-negative cases were labelled STEMI, whereas 15 delayed STE-positive cases were labelled NSTEMI. In regression analysis, D2B < 120 min remained the sole independent predictor of discordance (adjusted OR 6.7, 95% CI 3.5–13.8). Conclusions: In this registry, the cath-lab label “STEMI” showed the strongest correlation with meeting a 120 min benchmark, exceeding correlations for STE or angiographic occlusion. These findings suggest that quality-metric compliance, rather than electrocardiographic or anatomic criteria, predominantly drives final diagnosis. Full article

Background: Intracranial atherosclerosis disease (ICAD) represents a significant etiology of stroke. This study aimed to evaluate correlations between intracranial atherosclerotic burden and risk of ischemic events. Methods: In this prospective observational study, all enrolled patients underwent High-Resolution Magnetic Resonance vessel wall Imaging (HR MR-VMI) within two weeks of onset, or of enrollment. Baseline assessments included modified American Heart Association plaque type, stenosis degree, intra-plaque hemorrhage (IPH), plaque thickness, plaque length, and vessel wall enhancement. Modified Rankin Scale (mRS) was followed with one-year treatment in adherence to the guidelines. Comparative analyses were conducted between symptomatic and asymptomatic groups, culprit versus non-culprit plaques, and favorable versus poor prognosis groups. Results: The study included 129 symptomatic and 42 asymptomatic patients. Hypertension, diabetes, and smoking were more prevalent in patients in the symptomatic group. Vulnerable plaque (97.7% vs. 64.3%, p = 0.003), IPH (17.8% vs. 4.8%, p = 0.022) and higher stenosis degree (χ² = 2.675, p = 0.008) were significantly more prevalent in the symptomatic group. Culprit plaques were predominantly located in the superior wall of the middle cerebral artery (MCA) (χ² = 15.561, p = 0.001) and the left wall of the basilar artery (χ² = 34.138, p = 0.008). Factors associated with poor prognosis included older age (63.63 ± 8.19 vs. 55.63 ± 13.15, p = 0.001), presence of IPH (31.82% vs. 14.29%, p = 0.037), and elevated D-dimer levels (0.77 ± 0.60 vs. 0.40 ± 0.36, p = 0.022). Conclusions: Vulnerable plaque, specific lesion locations, and higher stenosis degree are significantly associated with ischemic events in ICAD. While plaque enhancement and stenosis correlate with stroke occurrence, they show no clear association with prognosis. Neither the length nor the thickness of plaques manifests a significant correlation with either stroke events or the prognostic outcomes. Full article

Introduction: Coronary artery disease remains one of the most prevalent causes of hospital cardiac arrest (OHCA). Although the benefit of early coronary angiography is well stablished in patients with ST-segment elevation, the benefit and the timing of performing it in other patients remain a matter of debate. This is due to the difficulty of identifying those in which an infarction with non-ST-segment elevation is the cause of the OHCA. Coronary artery calcium (CAC) emerges as a reliable predictor of coronary disease and adverse cardiovascular events, detectable even in non-gated chest computed tomography (CT) scans commonly used in OHCA etiological studies, showcasing potential for streamlined risk assessment and management. Aim: The aim of this study was to evaluate if CAC in non-gated CT scans performed in OHCA survivors could act as a good predictor of coronary artery disease on coronary angiography. Methods: This is a single-center, retrospective study of OHCA survivors without ST-segment elevation at presentation. We selected patients for whom a non-gated chest CT was performed and underwent coronary angiography due to the clinical, electrocardiogram (ECG), or echocardiographic suspicion of acute coronary syndrome. An investigator, blinded to the coronary angiography report, evaluated CAC both quantitively (with Agatston score) and qualitatively (visual assessment: absent, mild, moderate, or severe). Results: A total of 44 consecutive patients were included: 70% male, mean age of 60 ± 13 years old. The mean Agatston score was 396 ± 573 AU (Agatston units). Regarding the qualitative assessment, CAC was classified as mild, moderate, and severe in 11%, 25%, and 20% of patients, respectively. The coronary angiography revealed significant coronary lesions in 15 patients (34%), of which 87% were revascularized (80% underwent PCI and 7% CABG). The quantitative CAC assessment accurately predicted the presence of significant lesions on coronary angiography (AUC = 0.90, 95% CI 0.81–0.99, p < 0.001). The presence of moderate or severe CAC by visual assessment also predicted significant lesions on coronary angiography (OR 2.66, 95% CI 1.87–109.71, p = 0.01). There was also a good and significant correlation between the vessel with severe calcification in the CT scan and the culprit vessel evaluated by coronary angiography. CAC was reported in only 16% of the reviewed CTs, most of them with severe calcification. Conclusion: The assessment of CAC in non-gated chest CT scans proved to be feasible and displayed a robust correlation with the presence, severity, and location of coronary artery disease. Its routine use upfront was shown to be an important complement to CT scan reports, ensuring more precise and personalized OHCA management. 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: The identification of the left anterior descending (LAD) artery as the culprit vessel in ST-segment elevation myocardial infarction (STEMI) is critical for rapid decision-making and targeted reperfusion. Electrocardiography (ECG) remains a vital diagnostic tool, especially in cases of no prior clinical or imaging data. This study evaluates the accuracy of 12-lead ECG in identifying LAD involvement and occlusion level, while examining the prognostic significance of proximal versus distal LAD lesions in the era of modern reperfusion techniques. Methods: Data from 382 patients with STEMI were analyzed, focusing on the correlation between specific ECG patterns, particularly ST-segment elevation in aVL and aVR, and coronary angiographic findings. The predictive performance of ECG in localizing proximal LAD lesions was assessed through sensitivity, specificity, and predictive values. Clinical outcomes at 30 days and 2.5 years were compared between patients with proximal and distal LAD occlusions. Results: ST-segment elevation ≥ 0.5 mm in aVL or elevation in aVR, when associated with elevation in at least two contiguous precordial leads (V2–V4), demonstrated good sensitivity and predictive value for proximal LAD occlusion. Contrary to earlier studies, no significant difference in short- or long-term clinical outcomes was observed between proximal and distal LAD occlusion groups, possibly reflecting improvements in percutaneous coronary intervention (PCI) techniques and modern pharmacotherapy. Conclusions: The 12-lead ECG remains a valuable tool for identifying LAD as the culprit artery and approximating lesion location. However, in the era of advanced reperfusion therapy, the prognostic value of proximal LAD occlusion may be less pronounced than previously thought. These findings support a nuanced interpretation of ECG in guiding acute management without overestimating the long-term prognostic weight of lesion location alone. Full article

Fractional flow reserve (FFR) is a standard physiological index for guiding coronary revascularization, with a threshold of >0.80 typically used to defer intervention. However, due to its distinct anatomical and physiological features, the left anterior descending artery (LAD) often exhibits lower FFR values than non-LAD vessels for lesions of similar angiographic severity. These vessel-specific differences raise concerns about applying a uniform FFR cutoff across all coronary territories. Observational studies indicate that LAD lesions deferred at an FFR of 0.80 may have similar or better outcomes than non-LAD lesions do. LAD lesions also tend to show lower post-percutaneous coronary intervention FFR values, suggesting that vessel specific target thresholds may be more prognostically appropriate. Additionally, some evidence suggests that instantaneous wave-free ratio may offer greater prognostic value than FFR, specifically in LAD lesions, a trend not consistently seen in other arteries. In patients with acute myocardial infarction and multivessel disease, the prognostic relevance of non-culprit lesion FFR may vary by coronary territory, particularly in the LAD. This review outlines the physiological rationale and clinical evidence for vessel-specific interpretation of FFR, with a focus on the LAD, and explores its potential clinical implications and limitations. 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

Background: Residual risk after acute coronary syndromes (ACSs) continues to affect prognosis. We investigated the impact of female sex, non-ST-segment–elevation myocardial infarction (NSTEMI), diabetes mellitus (DM), and chronic kidney disease (CKD) on coronary atherosclerosis extent, culprit stenosis location, and bio-humoral data. The rate of both major adverse cardiovascular events (MACE) and non-fatal recurrent coronary events (RCE) was additionally evaluated. Methods: We enrolled 1404 ACS patients and followed them for up to 5 years. Coronary culprit and non-culprit stenoses were analyzed using angiography. Biohumoral data was assessed at admission and at 1 month and 12 months after discharge. Patients were compared based on sex, NSTEMI, DM, and CKD presence. Results: NSTEMI patients had a higher number of total coronary stenoses (3.5 vs. 3.3, p = 0.013) and non-culprit stenoses (2.3 vs. 1.6, p = 0.0001). Non-culprit percent stenosis was significantly greater in NSTEMI as compared to STEMI patients (57.9% vs. 47.1%, p = 0.0001). DM patients had a higher frequency of bifurcation lesions (41% vs. 25%, p = 0.0001). CKD patients showed a higher prevalence of left main disease (3.4% vs. 1.5%, p = 0.038). Female patients had higher LDL-cholesterol values at 1 month and 12 months. NSTEMI, DM, and creatinine level were independent predictors of MACE. NSTEMI patients had an increased risk of non-fatal RCE. Conclusions: NSTEMI, DM, and creatinine levels at admission were independent predictors of MACE in the first 5 years after an ACS. Full article

Most DNA damage caused by oxidative metabolism consists of single lesions that can accumulate in tissues. This review focuses on two classes of lesions: the two 8-oxopurine (8-oxo-Pu) lesions that are repaired by the base excision repair (BER) enzyme and the four 5′,8-cyclopurine (cPu) lesions that are repaired exclusively by the nucleotide excision repair (NER) enzyme. The aim is to correlate the simultaneous quantification of these two classes of lesions in the context of neurological disorders. The first half is a summary of reactive oxygen species (ROS) with particular attention to the pathways of hydroxyl radical (HO^•) formation, followed by a summary of protocols for the quantification of six lesions and the biomimetic chemistry of the HO^• radical with double-stranded oligonucleotides (ds-ODN) and calf thymus DNA (ct-DNA). The second half addresses two neurodegenerative diseases: xeroderma pigmentosum (XP) and Cockayne syndrome (CS). The quantitative data on the six lesions obtained from genomic and/or mitochondrial DNA extracts across several XP and CS cell lines are discussed. Oxidative stress contributes to oxidative DNA damage by resulting in the accumulation of cPu and 8-oxo-Pu in DNA. The formation of cPu is the postulated culprit inducing neurological symptoms associated with XP and CS. Full article

Background/Objectives: Drug-eluting stents (DESs) remain the standard of treatment for patients with ST-elevation myocardial infarction (STEMI). However, complications such as stent thrombosis and in-stent restenosis still pose significant risks. Drug-coated balloons (DCBs) have emerged as a promising alternative, but data for this clinical scenario are still scarce. The objective was to evaluate the safety and efficacy of DCB culprit-lesion primary percutaneous coronary intervention (pPCI) in patients presenting with STEMI and to evaluate its impact on the microcirculatory territory. Methods: An observational retrospective study was conducted across six European centers. Results: In total, 118 patients were included. Of these, 82.2% were male, with a median age of 67 years (IQR 36–92); 28% patients presented with stent thrombosis and most of them (94%) underwent paclitaxel-DCB-pPCI. The median follow-up was 23.2 months (IQR 6.7–77.3). Target lesion failure (TLF) rates were low (3.4%), with no differences between patients presenting with native coronary vessel and stent thrombosis (4.7% vs. 0%; p = 0.205). Overall mortality rates at follow-up were 7%, with only 1.8% attributed to cardiac causes. A target lesion revascularization (TLR) rate of 1.8% was observed, with no target vessel myocardial infarction reported. A subgroup of patients (42; 35.6%) underwent an adenosine-free angiographic microvascular resistance (AMR) analysis. The median AMR was 4.7 (3.9–5.5) and was greater in the stent thrombosis group than in the native coronary group (5.1 vs. 4.6; p = 0.038) with no clinical differences between patients based on the AMR. Conclusions: DCB-pPCI has emerged as an alternative potential treatment for patients presenting with STEMI, with few long-term adverse cardiac events. Despite the encouraging outcomes, these findings underscore the need for a large randomized clinical trial powered by a relevant clinical outcome in order to elucidate the role of DCB-PCI in patients presenting with STEMI. Full article

Chronic rhinosinusitis (CRS) is a common inflammatory disease of the paranasal sinuses with a yet unknown etiology. As studies continue to elucidate the disease’s heterogeneity inflammatory profile and presentation, there is a growing interest in the influence of the nasal microbiome on disease pathogenesis and chronicity. The sinus microbiota appear dominated by the Staphylococcus and Corynebacterium genera; known upper airway pathogens, such as Haemophilus influenza, are present in the upper airways of healthy individuals, though at relatively lower abundances than in CRS patients. Viral culprits may induce an unhindered local immune response that contributes to the recurrence and chronicity of inverted papillomas—benign mucosal lesions with the propensity for local destruction and malignant transformation that can be found in patients with a history of nasal infection. The persistence of inverted papillomas warrants investigation into their pathogenesis and how they may contribute to a nasal landscape promoting the chronicity of CRS. Further investigation is needed to uncover the interplay between resident microbiota and viral, fungal, and immunological influence. Discerning between ‘healthy’ and ‘diseased’ sinonasal microbiomes and ‘keystone’ species could shed light on CRS etiology and provide the opportunity for CRS treatment tailored to an individual’s microbiome. This review aims to explore the interrelation of microbial residents in the pathogenesis and chronicity of the diseased sinonasal environment. Full article

Background/Objectives: Troponin level elevation without an obstructive culprit lesion is caused by heterogenous entities. The effect of aging on this condition has been poorly investigated. Methods: After screening 24,775 patients between 2010 and 2021, this study included a total of 373 patients with elevated troponin levels without an obstructive culprit lesion or suspected myocardial infarction with non-obstructive coronary arteries (MINOCAs) categorized into four age groups containing 78 patients (<51 years), 72 patients (51–60 years), 81 patients (61–70 years), and 142 patients (>70 years). This study analyzed the baseline characteristics, the in-hospital complications, in-hospital mortality, and the long-term outcomes. Results: The older patients exhibited a higher rate of major adverse cardiovascular in-hospital events than those of the other age groups (15.4% in the <51-year-old group vs. 36.1% in the 51–60-year-old group vs. 33.3% in the 61–70-year-old group vs. 47.2% in the >70-year-old group; p < 0.001). However, the rate of non-sustained ventricular tachycardia (nsVT) was higher in the 51–60-year-old patients than those of the other age groups (5.6% in the 51–60-year-old group vs. 1.3% in the 61–70-year-old group vs. 0.7% in the >70-year-old group; p = 0.027). At the 11-year follow-up, cardiovascular mortality was higher among the older patients compared to that of the younger patients (3.9% in the 61–70-year-old group vs. 4.2% in the >70-year-old group, p = 0.042), while non-cardiovascular mortality was comparable between the age groups. Conclusions: The older patients with troponin level elevation without an obstructive culprit lesion experienced a higher incidence of major adverse cardiovascular events during hospitalization compared to that of the younger groups. Additionally, higher cardiovascular mortality rates were revealed in the older patients at a long-term follow-up. Full article

Background: ST-segment elevation myocardial infarction (STEMI) remains a leading cause of mortality worldwide, primarily caused by acute thrombosis over atherosclerotic plaques. Simultaneous acute thrombosis in two coronary arteries is an exceptionally rare event. This report highlights a unique case of STEMI associated with cardiogenic shock due to dual coronary artery thrombosis and provides insights from a literature review on this rare condition. Methods: We report the case of a 58-year-old male with a history of hypertension, type II diabetes, and heavy smoking, who presented with a two-day history of chest pain and cardiogenic shock. Diagnostic evaluation included an electrocardiogram showing ST-segment elevation in AVR and ischemia, along with echocardiography revealing severe left ventricular dysfunction (ejection fraction 20%). Emergency coronary angiography was performed to identify the underlying pathology. Additionally, a literature review was conducted to analyze the characteristics and outcomes of similar cases of dual coronary artery thrombosis. Results: Coronary angiography identified significant occlusions in the proximal circumflex branch and the left anterior descending artery (LAD), a combination rarely reported in the literature. Our review confirmed that dual thrombosis involving the LAD and right coronary artery (RCA) is the most frequently described presentation of this condition, while simultaneous CFX and LAD thrombosis is exceedingly rare. Most reported cases, including ours, were associated with cardiogenic shock, highlighting the severity of this clinical entity. Despite successful thrombus aspiration and stenting, our patient experienced severe complications, including infections, pleural effusions, and paralytic ileus, ultimately requiring evaluation for left ventricular assist device implantation. Conclusions: This case underscores the complexity and critical challenges of managing STEMI with cardiogenic shock due to simultaneous coronary thrombosis. The findings from our literature review suggest the need for heightened clinical awareness and tailored revascularization strategies. Further studies are warranted to optimize management approaches and improve outcomes in such rare and high-risk scenarios. Full article

Diagnosis and treatment of acute coronary syndrome (ACS) pose particular challenges in elderly patients. When high troponin levels are detected, the distinction between non-ischemic myocardial injury (NIMI), type 1, and type 2 myocardial infarction (MI) is the necessary first step to guide further care. However, the assessment of signs of ischemia is hindered in older patients, and no simple clinical or laboratory tool proved useful in this discrimination task. Current evidence suggests a benefit of an invasive vs. conservative approach in terms of recurrence of MI, with no significant impact on mortality. In patients with multivessel disease in which the culprit lesion has been treated, a physiology-guided complete percutaneous revascularization significantly reduced major events. The management of ACS in elderly patients is an example of the actual need for a multimodal, thorough clinical approach, coupled with shared decision-making, in order to ensure the best treatment and avoid futility. Such a need will likely grow throughout the next decades, with the aging of the world population. In this narrative review, we address pivotal yet common questions arising in clinical practice while caring for elderly patients with ACS. Full article