Search Results (4,264)

The evaluation of stents in coronary computed tomography angiography (CCTA) is still a major topic in cardiovascular imaging. Using Photon-Counting Detector CT (PCCT) may improve the assessment of coronary stents and make on-site CT-FFR analysis feasible for ruling out in-stent restenosis (ISR). In this study, patients with previous coronary stent implantation who underwent CCTA using PCCT and subsequent invasive catheter angiography (ICA) were included. Stent characteristics such as location and length were reported. CT-FFR measurements were taken 1.8 cm before and after the stent, with a value of ≤0.80 defined as hemodynamically significant under respecting the diagnostic accuracy drop in the gray zone between 0.76 and 0.80. Delta CT-FFR with a cut-off value of ≥0.06, indicating hemodynamic significance, was determined. Any ISR and interventional treatment during the following ICA was recorded. Diagnostic performance metrics, including sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV), were calculated for post-stent CT-FFR and Delta CT-FFR in detecting ISR. Patients were followed up to evaluate the rate of major adverse cardiovascular events (MACE) 6 months after CCTA. A total of 19 patients (5 female, 14 male, median age 69 years) were enrolled in this study. In most cases, coronary stents were located in the proximal LAD with a median stent length of 70.2 mm. Pathological CT-FFR < 0.76 distal to the stent was detected in 6 cases (31.6%), while pathological Delta CT-FFR ≥ 0.06 occurred in 14 cases (73.7%). ICA was performed in three of these patients, with ISR confirmed in two cases. These findings yield sensitivity and NPV of 100% for both post-stent CT-FFR and Delta CT-FFR for excluding ISR with a superior specificity (76.5% vs. 29.4%) and overall diagnostic accuracy (78.9% vs. 36.8%) for post-stent CT-FFR. Two patients reported a myocardial infarction in follow-up; however, neither of them was located in the territory of the stented coronary artery. This study outlines the feasibility of on-site CT-FFR analysis using PCCT in excluding ISR in coronary stents with a high diagnostic accuracy. These findings highlight the need to extend the benefits of CT-FFR analysis for non-invasive assessment of possible ISR regarding personalized risk stratification and therapy planning. Full article

Atherosclerosis is a chronic multifactorial inflammatory vascular disease and the major risk factor for cardiovascular diseases (CVDs), characterized by arterial wall thickening, loss of arterial elasticity and the progressive accumulation of lipids and immune cells, ultimately leading to plaque formation and the development of unstable, rupture-prone plaques. Several studies suggest that gut microbiota might contribute to atherosclerosis, mainly by converting dietary and endogenous molecules into bioactive metabolites, such as trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and the Gram-negative cell-wall component lipopolysaccharide (LPS). Such metabolites can promote key mechanisms involved in the development and progression of atherosclerotic plaque, and, importantly, plaque vulnerability. Specifically, they can worsen endothelial dysfunction, induce macrophage-driven inflammatory responses, and cause oxidative stress and extracellular matrix degradation. These processes are crucial for thinning of the fibrous cap and destabilization of atherosclerotic plaques. As a result, the risk of plaque rupture and related cardiovascular events increases. In this review, we summarize potential mechanisms by which the gut microbiota and their compounds induce the formation of vulnerable atherosclerotic plaques and discuss findings from experimental models and clinical studies that reveal the crucial role of microbiota–host dynamics in atherosclerosis. In contrast to previous reviews that primarily focused on atherosclerosis development, we specifically highlight the cellular and molecular mechanisms linking gut microbiota to plaque vulnerability and destabilization. We also address future research priorities to define microbiota-driven pathways better and develop targeted therapeutic interventions to reduce plaque vulnerability and cardiovascular risk. Full article

Background: Patients with coronary heart disease (CHD) complicated by diabetes mellitus (DM) remain at substantial residual cardiovascular risk despite contemporary guideline-directed medical therapy. However, the long-term trajectory of this excess risk and its temporal pattern have not been fully clarified. Methods: This is a retrospective cohort study based on a large-scale public database and real-world clinical data. The primary cohort was derived from the UK Biobank (UKB), including 7491 CHD patients and 2322 CHD with DM patients; the validation cohort included 362 CHD patients from Tongji Hospital. Both cohorts were followed for up to 10 years, with major adverse cardiovascular events (MACE) as the primary endpoint. Propensity score matching (PSM) was employed to balance baseline confounders. Kaplan–Meier analysis combined with piecewise log-rank tests were used to assess cumulative risk differences at various follow-up time points. Multivariable Cox proportional hazards models were constructed to evaluate the independent impact of diabetes. Results: In the UKB cohort, CHD with DM patients exhibited significantly higher risks of MACE and cardiovascular death before matching. After 1:1 PSM, no significant difference in MACE risk was observed during the early follow-up period (1 year, p > 0.05). However, survival curves showed progressive divergence over time, with the risk difference reaching statistical significance at 10 years (p = 0.0004), demonstrating a pronounced time-cumulative effect. The Tongji validation cohort similarly confirmed that event-free survival was significantly lower in the CHD with DM group (p = 0.0028). Independent risk factor analysis using multivariable Cox regression showed that after adjusting for age, sex, smoking, and lipid parameters, diabetes remained an independent risk factor for long-term MACE (UKB cohort HR > 1; Tongji cohort HR = 1.86, 95% CI: 1.20–2.86, p = 0.005). Conclusions: Diabetes significantly increases the long-term residual cardiovascular risk in CHD patients. This excess risk is characterized by a clear time-cumulative effect: under modern guideline-directed medical therapy, early risk may be effectively buffered, but long-term adverse events remain markedly elevated. More proactive and intensified long-term intervention strategies are urgently needed for CHD patients with comorbid diabetes. Full article

Accurate R-peak detection in electrocardiogram (ECG) signals is fundamental for cardiovascular analysis. However, most existing methods address differences in sampling frequency (f_s) through signal resampling or transfer learning, which may alter the temporal definition of annotated events. In this study, we propose a f_s consistent framework for ECG R-peak detection that avoids both resampling and retraining. The proposed method is based on low-sampling morphological learning combined with physiological temporal constraints (PTC). A lightweight classifier based on Extreme Gradient Boosting (XGB) was trained on 128-Hz ECG data from the MIT-BIH Normal Sinus Rhythm Database to learn local morphological structures, and feature extraction is defined in milliseconds with time-normalized derivatives to ensure consistency across f_s. The trained model is directly applied to higher-f_s datasets (360 Hz, 500 Hz, and 1000 Hz) without modification. Final peak locations are determined through deterministic processing, including PTC and local snap processing. Experimental results demonstrated that the proposed method achieved stable detection performance across multiple sampling frequencies. When evaluated in a sample-wise manner, the proposed method achieved mean F1-scores of 0.885 on MIT-BIH Arrhythmia Database (360 Hz), 0.848 on Lobachevsky University Electrocardiography Database (LUDB, 500 Hz, sinus rhythm), 0.837 on LUDB (500 Hz, arrhythmia), and 0.953 on PTB Diagnostic ECG Database (1000 Hz), without any resampling or retraining. The integration of probabilistic candidate detection and deterministic temporal alignment enables consistent peak localization under cross-frequency conditions. These findings demonstrate that augmenting machine learning with deterministic decision mechanisms provides a principled framework for f_s-consistent ECG peak detection. Full article

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have rapidly evolved from glucose-lowering agents to central players in cardiovascular risk reduction. Evidence from landmark randomized controlled trials has established their capacity to reduce major adverse cardiovascular events, promote anti-inflammatory signaling, attenuate ischemia–reperfusion injury, and improve myocardial metabolic efficiency. As the prevalence of obesity, type 2 diabetes mellitus, and heart failure in the cardiac surgical population grows, GLP-1 RAs are increasingly encountered in the perioperative setting. Yet the cardiac surgery literature has yet to synthesize their emergent role coherently. This is a narrative review; no systematic review or meta-analysis was performed. This narrative review integrates mechanistic, clinical, and translational evidence to reframe GLP-1 RAs as potential perioperative cardioprotective agents in patients undergoing cardiac surgery. We examine receptor-level biology, evidence from the GLOBE randomized trial, observational data linking GLP-1 RA use to reduced postoperative atrial fibrillation after coronary artery bypass grafting, the rationale for the forthcoming REVERSE-TAVR trial, and evolving perioperative management guidelines. Key evidence gaps are identified, including the absence of prospective data in open cardiac surgery, aortic surgery, and high-acuity populations. We propose a research agenda and conceptual framework to guide future investigation into GLP-1 RAs as a new dimension of perioperative cardioprotection. The current evidence is hypothesis-generating; a definitive perioperative cardioprotective benefit has not yet been demonstrated in cardiac surgery populations, and these agents are presented here as potential rather than proven cardioprotective tools. Full article

Background: Intensive low-density lipoprotein cholesterol (LDL-C) reduction is essential for secondary prevention after acute coronary syndrome (ACS). Although randomized trials support the use of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, real-world evidence on long-term lipid control and the optimal timing of initiation remains limited. Objective: To evaluate lipid outcomes and atherosclerotic cardiovascular disease (ASCVD) events associated with evolocumab after ACS and to assess whether timing of initiation influences these outcomes in routine clinical practice. Methods: This multicenter, retrospective cohort study included adults who were initiated on evolocumab following ACS between 2017 and 2024. Lipid parameters were assessed at predefined follow-up time points (3 months, 6 months, 1 year, 2 years, and up to 3 years) using an available-case approach. Patients were categorized as early initiators (≤1 month) or late initiators (>1 month). Recurrent ASCVD events, hospitalization burden, and mortality were analyzed using multivariable regression. A propensity score-matched sensitivity analysis was also performed. Results: Among 525 included patients (mean age 53.1 ± 11.6 years; 80.2% male), baseline LDL-C was 3.68 ± 1.66 mmol/L. LDL-C decreased to approximately 1.8–2.0 mmol/L within 3 months, corresponding to an approximate 45–50% reduction from baseline, with consistent reductions observed across available follow-up time points. Recurrent ASCVD events occurred in 14.8% of patients, and in-hospital mortality was 2.3%. Although early initiators had higher baseline risk, adjusted analyses showed no statistically significant association between early initiation and recurrent ASCVD (adjusted OR 1.50; 95% CI 0.82–2.70; p = 0.17). Similarly, no statistically significant differences in lipid outcomes were observed between early and late initiation groups after adjustment. Findings were consistent in propensity score-matched analyses. Conclusions: In this real-world post-ACS cohort, evolocumab was associated with substantial and sustained LDL-C reduction across follow-up time points. No significant associations were observed between timing of initiation and lipid or ASCVD outcomes after adjustment. These findings should be interpreted cautiously, given the observational design, available-case analysis, and potential for residual confounding. Full article

Background: Low high-density lipoprotein cholesterol (HDL-C) is an established marker of cardiovascular risk. However, HDL-C levels may change over time in relation to metabolic status, lifestyle factors, and medication use, and the cardiovascular implications of longitudinal HDL-C changes remain incompletely understood. Methods: We conducted a retrospective cohort study using the JMDC Claims Database, including 3,387,924 adults who underwent at least two health checkups between 2005 and 2021. Participants were categorized into four groups based on HDL-C changes between two time points: persistently low, low to normal, normal to low, and persistently normal. The primary outcome was incident composite cardiovascular disease (CVD), including myocardial infarction, angina pectoris, stroke, heart failure, and atrial fibrillation. Cox proportional hazards models were used to estimate hazard ratios (HRs) with adjustment for demographic and clinical covariates. Results: During a mean follow-up of 4.3 years, persistently low HDL-C was associated with the highest risk of composite CVD compared with persistently normal HDL-C (HR 1.15, 95% CI 1.12–1.19). Both Low-to-Normal and Normal-to-Low groups also showed elevated risks (HR 1.10, 95% CI 1.06–1.14; HR 1.14, 95% CI 1.10–1.19, respectively). The strongest association was observed for myocardial infarction, whereas the association with stroke was modest and less consistent after full adjustment. Conclusions: Longitudinal changes in HDL-C were associated with cardiovascular risk after adjustment for cardiometabolic factors and medication use. Persistently low HDL-C conferred the greatest risk, and serial HDL-C patterns may provide additional information for cardiovascular risk assessment beyond a single baseline measurement. Full article

Background/Objectives: Contemporary heart failure (HF) guidelines recommend early initiation of four foundational drug classes in HFrEF. However, real-world prescription rates of guideline-directed medical therapy (GDMT) at discharge remain low, and comparative data in this setting is limited. We aimed to explore the association between GDMT intensity prescribed at or before hospital discharge and clinical outcomes. Methods: MEDLINE and EMBASE were searched through March 2026 (PROSPERO CRD420261352137). A frequentist random-effects network meta-analysis grouped regimens into four intensity nodes (single/none, double, triple, quadruple), with the primary analysis restricted to adjusted hazard ratios. The primary outcome was the composite of all-cause mortality (ACM) and HF hospitalization (HFH). Secondary outcomes were HFH alone, ACM, and cardiovascular mortality. Confidence was rated with CINeMA. Estimates are reported as associations, not treatment effects. Results: Twenty-seven studies (26 observational, 1 RCT; 73,174 patients) were included. Among SGLT2i-era cohorts, quadruple therapy was suboptimally prescribed (pooled 34%, range 11.6–55.2%). For the primary composite endpoint, more complete regimens were associated with progressively lower event rates versus single or no therapy (double: hazard ratio 0.76, 95% CI 0.68–0.84; triple: 0.72, 0.64–0.81; quadruple: 0.52, 0.36–0.75; τ² = 0). A consistent ordinal gradient was seen across outcomes, with quadruple therapy ranking first numerically for every outcome in which it was estimable. The direction and ordering were preserved in a sensitivity analysis additionally incorporating risk ratios, on stratification by follow-up duration, and in an alternative network anchored to incomplete therapy. Because most evidence was observational, the magnitude of these associations should not be interpreted as a causal treatment effect and likely reflects residual confounding and selection bias. Conclusions: Discharge GDMT remains an important opportunity to improve outcomes in patients with HF. Adequately powered randomized trials are required to establish the incremental benefit of this approach and to close the gap between evidence and practice. Full article

Current acute coronary syndrome (ACS) care relies on sequential, single-modality diagnostics, in which the electrocardiogram, the troponin trajectory, and the coronary angiogram are interpreted independently rather than as a joint signal. This narrative review maps rather than pools the evidence. We selectively searched PubMed, EMBASE, Cochrane CENTRAL, and Web of Science (January 2015–February 2026); study selection was performed by a single reviewer, without duplicate screening, a PRISMA flow diagram, or a formal risk-of-bias assessment. The three key findings are as follows: A machine learning-enabled electrocardiogram (ECG) for diagnosing occlusion due to myocardial infarction achieved an AUC of 0.938 (95% CI = 0.924–0.951) on data not seen during training and correctly diagnosed 42% of patients that expert interpreters missed. A machine learning-enabled high-sensitivity troponin interpretation method, CoDE-ACS, reported an AUC of 0.953 and increased the number of patients ruled out at initial evaluation from 27% to 61%. Angiographically derived physiological methods produced conflicting results—quantitative flow ratios reduced major adverse cardiovascular events (MACE) in the FAVOR III China trial (HR 0.65), but in FAVOR III Europe the angiography-derived approach did not prove non-inferior to FFR; if anything, QFR guidance led to more events (6.7% vs. 4.2%, an event rate about 60% higher in the QFR arm; HR 1.63; 95% CI 1.11–2.41). There was no difference between FFR-angio and FFR in the ALL-RISE trial. These are diagnostic-accuracy and prognostic-association findings; no trial has yet shown that AI-guided ACS care reduces death, reinfarction, or ischemia-driven revascularization. Full article

Myocardial ischemia–reperfusion injury (MIRI) represents a major contributor to morbidity and mortality in patients undergoing reperfusion therapy after acute myocardial infarction. Although timely restoration of coronary blood flow is essential for myocardial salvage, reperfusion paradoxically initiates a complex cascade of molecular and cellular events that may aggravate myocardial injury. Oxidative stress is considered one of the central mechanisms underlying MIRI, primarily through excessive production of reactive oxygen species (ROS) and reactive nitrogen species (RNS), leading to mitochondrial dysfunction, calcium overload, endothelial injury, inflammatory activation, and cardiomyocyte death. This review summarizes the current understanding of the pathophysiological mechanisms involved in oxidative stress-mediated reperfusion injury, with emphasis on mitochondrial permeability transition pore opening, inflammasome activation, cytokine release, neutrophil extracellular trap formation, macrophage polarization, and interconnected cell death pathways including PANoptosis. Emerging evidence regarding immunometabolic regulation and epigenetic modulation in MIRI is also discussed. In addition, current pharmacological and non-pharmacological cardioprotective strategies targeting oxidative stress, mitochondrial dysfunction, and inflammatory signaling are reviewed, highlighting both promising experimental findings and the persistent challenges in clinical translation. A deeper understanding of the molecular interplay between oxidative stress and inflammatory pathways may facilitate the development of integrated therapeutic approaches aimed at improving myocardial recovery and long-term cardiovascular outcomes following reperfusion therapy. Full article

Background: Lowering low-density lipoprotein cholesterol (LDL-C) effectively reduces the risk of cardiovascular events. Therefore, we investigated LDL-C levels in geriatric patients undergoing comprehensive inpatient geriatric care. Methods: Patients aged ≥65 years who underwent inpatient comprehensive geriatric care were analyzed. Baseline, clinical, laboratory, and medical data were obtained from case records. For cardiovascular risk stratification, SCORE2, SCORE2-OP, or SMART2 was applied, and LDL-C targets for primary or secondary prevention of atherosclerotic cardiovascular disease (ASCVD) were defined. Factors associated with LDL-C values within guideline-recommended targets in the univariate analysis were entered into a logistic regression model to identify independent predictors. Results: Of 486 patients, 433 (median age 84.0 years; 67.2% female) were included in the final analysis. The majority of patients (371/433; 85.7%) had a very high cardiovascular risk profile. Lipid-lowering therapy (LLT) was identified in 222 patients (51.3%), while 205 patients (47.3%) had received LLT for ≥3 months. In 219 patients (98.7%), LLT was statin-based, either as monotherapy or in combination. The median LDL-C level in the entire cohort was 85 mg/dL (IQR: 63–114 mg/dL), whereas patients receiving LLT had a median LDL-C level of 66 mg/dL (IQR: 52–83 mg/dL). Overall, 193 patients (44.6%) achieved guideline-recommended LDL-C targets; among patients receiving LLT, 61.5% (126/205) were within target range. Intake of ≥5 medications per day was associated with pre-existing LLT (odds ratio: 3.036; 95% CI: 1.081–8.523; p = 0.035). Statin-based LLT was independently associated with achieving LDL-C targets (odds ratio: 3.383; 95% CI: 2.248–5.092; p < 0.001). Conclusions: Most patients did not achieve guideline-recommended LDL-C targets, while only half received lipid-lowering therapy, predominantly statin-based. Current risk assessment tools and approaches to polypharmacy may require adaptation for geriatric patients. Nevertheless, even the simple implementation of statin therapy alone could substantially improve cardiovascular preventive care in a large proportion of untreated older patients. Full article

Background: Older adults undergoing non-cardiac surgery are vulnerable to perioperative complications, but the prognostic value of routine echocardiographic markers in high-acuity cohorts remains incompletely defined. Methods: This secondary analysis of a prospective cohort included 503 consecutive adults with known cardiovascular disease undergoing non-cardiac surgery, characterized by a high proportion of urgent presentations. Patients were stratified by age (geriatric, ≥65 years; non-geriatric, <65 years). The primary endpoint was major in-hospital adverse events (MIAEs), defined as a composite of in-hospital death, surgical reintervention, and postoperative acute kidney injury (AKI). Postoperative creatinine was not routinely measured in stable patients discharged early; therefore, renal outcomes were interpreted strictly as available-case analyses (n = 364). Results: MIAEs occurred more frequently in geriatric than in younger patients (45.5% vs. 30.8%). Within the geriatric cohort, patients with reduced LVEF (<50%) had lower MAPSE values and higher crude rates of AKI, death, and MIAE than those with LVEF ≥ 50%. In multivariable analyses, reduced LVEF was associated with MIAE, although this small subgroup was susceptible to statistical overfitting. MAPSE reflected longitudinal systolic dysfunction but did not retain independent prognostic value after adjustment. Conclusions: In this pilot subgroup analysis of high-acuity patients, reduced preoperative LVEF (<50%) served as a clinical flag identifying a high-risk geriatric phenotype with increased cardiorenal vulnerability. Given the event-enriched available-case denominator, these findings should be considered hypothesis-generating observations intended to increase clinical awareness. Full article

Coronary drug-eluting stents (DESs) are the current clinical standard, yet delayed endothelialization remains a critical challenge. Graphene-based coatings have emerged as promising cardiovascular biomaterials due to their favorable hemocompatibility and ability to support endothelial cell growth. In this study, we evaluated the in vivo performance of graphene-coated stents (GCSs) compared with commercial sirolimus-eluting stents in a Polish White swine model (n = 10). Stents were implanted into major coronary branches, with follow-up at 30 and 90 days using quantitative coronary angiography (QCA), optical coherence tomography (OCT), and cryogenic scanning electron microscopy (cryo-SEM). No systemic toxicity, mortality, thrombotic events, or ischemic complications were observed during the study period. QCA demonstrated no significant differences in percent diameter stenosis between GCSs and DESs at either 30 days (12.3 ± 6.1% vs. 8.6 ± 5.8%, p = 0.2782) or 90 days (18.3 ± 10.5% vs. 9.6 ± 6.6%, p = 0.1074). OCT analysis confirmed comparable lumen and neointimal parameters between groups, while demonstrating a favorable, although non-significant, trend toward a lower percentage of uncovered struts in GCSs. Cryo-SEM imaging demonstrated stable tissue integration and a preserved healing response surrounding GCSs. Collectively, these findings indicate that GCSs are safe and biocompatible and demonstrate mid-term vascular performance comparable to clinically used DES platforms. The presented results support further investigation of graphene-based coatings as potential surface-modification strategies for coronary stents. Full article

Background/Objectives: Antibody–drug conjugates (ADCs) have transformed the therapeutic landscape of breast cancer, expanding treatment opportunities across multiple disease settings. However, their increasing clinical use has revealed a heterogeneous spectrum of toxicities that extends beyond conventional chemotherapy-related adverse events. Emerging evidence suggests that ADC-associated toxicities are driven by a complex interplay between ADC structural characteristics, including target antigen expression, payload properties, linker stability, drug-to-antibody ratio, and patient-related susceptibility factors. This review aims to provide a comprehensive overview of ADC-related toxicities in breast cancer, integrating mechanistic insights with clinical management strategies and risk-adapted approaches. Methods: A narrative review of the literature was conducted focusing on clinical trials, real-world studies, translational investigations, and mechanistic evidence related to ADC-associated toxicities in breast cancer. Particular attention was given to the relationship between ADC design, toxicity mechanisms, patient-specific risk factors, and clinical management. Results: ADC-related toxicities encompass a broad range of adverse events, including hematologic toxicity, interstitial lung disease, gastrointestinal complications, hepatotoxicity, peripheral neuropathy, stomatitis, ocular toxicity, dermatologic adverse events, and cardiovascular manifestations. Current evidence indicates that toxicity profiles differ substantially across ADCs and are influenced by multiple factors, including payload class, linker chemistry, target biology, intracellular trafficking, bystander effects, systemic payload exposure, and host-related characteristics. While several toxicities can be anticipated through careful monitoring and early intervention, clinically significant variability remains, and validated predictive biomarkers are largely lacking. Emerging real-world evidence further highlights the importance of individualized toxicity assessment and multidisciplinary management. Conclusions: ADC-related toxicity should be viewed as a multifactorial biological process resulting from the interaction between ADC design and host susceptibility rather than as a uniform class effect. A mechanistic understanding of toxicity pathways may improve risk stratification, toxicity monitoring, and personalized management strategies. Future research should focus on the development of predictive biomarkers, pharmacologic risk models, and next-generation ADC platforms with improved therapeutic indices. This review proposes an integrated framework linking ADC structural determinants, toxicity mechanisms, and clinical management to support safer and more individualized use of ADCs in breast cancer. Full article

Myocardial infarction with non-obstructive coronary arteries (MINOCA) accounts for approximately 5–15% of all myocardial infarctions and disproportionately affects women. Once treated as a diagnosis of exclusion, MINOCA is now recognised as a heterogeneous, mechanism-based syndrome encompassing atherosclerotic plaque disruption, epicardial and microvascular vasospasm, microvascular dysfunction, coronary thromboembolism, and spontaneous coronary artery dissection (SCAD). Despite the absence of obstructive disease, it carries substantial morbidity and mortality, underscoring the need for accurate aetiological characterisation and tailored therapy. Our aim is to review the contemporary evidence of the role of advanced imaging modalities—cardiac magnetic resonance imaging (CMR), optical coherence tomography (OCT), intravascular ultrasound (IVUS) and invasive functional testing—in the diagnosis, prognostic stratification, and therapeutic guidance of patients with MINOCA. CMR is the non-invasive reference standard for differentiating true ischaemic MINOCA from non-ischaemic mimics such as myocarditis and Takotsubo syndrome, reclassifying the working diagnosis in up to two-thirds of cases. OCT and IVUS provide intracoronary characterisation of culprit substrates that are invisible via angiography, particularly plaque rupture, erosion, intramural haematoma and SCAD, while acetylcholine and adenosine testing identify endothelium-dependent vasospasm and endothelium-independent microvascular dysfunction respectively. Coronary Computed Tomography Angiography (CCTA) could also play an additional role in the diagnosis of epicardial CAD. Each modality additionally carries independent prognostic value, with abnormal findings consistently linked to higher rates of major adverse cardiovascular events. The recently completed PROMISE trial provided the first randomised evidence that stratified, imaging-guided treatment might have some positive impact on angina status and quality of life compared with empirical standard care. In conclusion, advanced imaging has transformed MINOCA from a diagnosis of exclusion into a mechanism-based syndrome amenable to personalised therapy. Broader integration of these modalities into routine practice, supported by further randomised trials, is needed to optimise outcomes. Full article