Myocardial infarction with non-obstructive coronary arteries (MINOCA) is a clinical entity characterized by the absence of significant coronary artery obstruction in epicardial arteries (<50%) on coronary angiography in the setting of acute myocardial infarction (AMI). This article aims to provide a narrative review of the pathophysiological mechanisms, diagnostic challenges, and prognosis associated with MINOCA based on pathophysiology regarding the atherosclerotic and non-atherosclerotic causes. Etiological factors, including thromboembolism, coronary artery spasm, spontaneous coronary artery dissection, coronary microvascular disease, and supply–demand mismatch, are addressed. Imaging modalities such as echocardiography, advances in coronary angiography like intravascular ultrasound (IVUS) and optical coherence tomography (OCT), cardiac magnetic resonance (CMR), and coronary computed tomography angiography (CCTA) are also analyzed. MINOCA patients have a better short-term prognosis compared to those with obstructive coronary artery disease but face significant long-term risks, underscoring the need for precise diagnosis and management strategies. Elevated inflammatory markers and specific genetic predispositions are also associated with adverse outcomes in MINOCA. This review focused on MINOCA from a pathophysiological perspective on the diverse underlying mechanisms, the challenges in achieving accurate diagnosis, the importance of a tailored therapeutic approach and the necessity for further investigation of clinical outcomes.

Background: the role of echocardiography in septic shock remains controversial, since depressed cardiac afterload may overestimate left ventricular (LV) systolic performance and mask septic cardiomyopathy (SC). We hypothesized that afterload-adjusted LV ejection fraction (LVEF) and LV outflow tract velocity-time integral (VTI) values for given systemic vascular resistances (SVR) could provide novel insights into recognizing and stratifying the severity of SC. Methods: in this observational, monocentric study, we prospectively included 14 mechanically-ventilated patients under septic-shock who all had a Pulse index Continuous Cardiac Output (PiCCO) system in place for hemodynamic monitoring. Echocardiographic and PiCCO longitudinal examinations (71 measurements overall) were performed simultaneously at the onset of septic shock and every 12 h for 60 h overall. Results: VTI-derived stroke volume (SV) and cardiac output (CO) were significantly correlated with PiCCO measurements (r ≥ 0.993, both p < 0.001). LVEF and VTI showed linear and exponential inverse correlation to SVR (R2 = 0.183 vs. 0.507 and p < 0.001 vs. p < 0.001, respectively). The equations LVEF = 86.168 − 0.011 × SVR and VTI = 41.23 × e^{(−0.0005×SVR)} were found to provide “predicted” values for given SVR. Measured to predicted LVEF ratios (for given SVR), the afterload-adjusted LVEF defined the severity of SC (mild ≥ 90%, 80% ≤ moderate < 90% and severe < 80%). Mild SC demonstrated normal/supra-normal LVEF, normal VTI and SVR. Moderate SC showed lower LVEF and SVR, yet increased LV end-diastolic volume (LVEDV), VTI, SV and CO compared with mild SC (all p < 0.05). Severe SC was distinguished from moderate SC by markedly reduced LVEF, LVEDV, VTI, SV, CO and significantly increased SVR (all p < 0.05). LVEF and VTI decreased over time in mild SC, LVEF decreased in moderate SC, and LVEF and VTI increased over time in severe SC (p ≤ 0.038). LVEF and VTI demonstrated significant performance in identifying severe SC [cut-off < 61.5%, area under the curve (AUC) = 1 ± 0.0, sensitivity/specificity = 100/100, p < 0.001 vs. cut-off < 17.9 cm, AUC = 0.882 ± 0.042, sensitivity/specificity = 80/77, p < 0.001, respectively]. VTI but not LVEF demonstrated significant diagnostic performance in identifying both SVR < 800 dynes·s·cm⁻⁵ and SVR > 1500 dynes·s·cm⁻⁵ (cut-off > 24.46 cm, AUC = 0.889 ± 0.049, sensitivity/specificity = 75/100, p < 0.001; cut-off < 16.8, AUC = 0.0.857 ± 0.082, sensitivity/specificity = 83/86, p = 0.002, respectively).Conclusions: our study suggests that ICU bedside echocardiographic assessment of LVEF, VTI and their adjusted to corresponding SVR values provides valuable insights for the comprehension of SC phenotypes, underlying vasoplegia and cardiac output fluctuations in septic shock.

Background: SCN5A mutations may present with different clinical phenotypes such as Brugada syndrome, long QT3 syndrome, sick sinus syndrome, atrial fibrillation, dilated cardiomyopathy, and the least known multifocal ectopic Purkinje-related premature contractions syndrome. Case summary: We report a case of a 29-year-old woman with palpitations due to multifocal premature ventricular complexes (PVCs) and a family history of sudden death. The previous electrophysiological study had shown that PVCs arose from Purkinje fibres but catheter ablation was unsuccessful. Cardiac magnetic resonance (CMR) imaging demonstrated non-ischaemic areas of subendocardial fibrosis at multiple left ventricular (LV) segments with concomitant dilatation and mild systolic impairment. Amiodarone suppressed the ectopy but caused hyperthyroidism. Due to recent pregnancy, she received no antiarrhythmics which resulted in PVC burden increase and further deterioration of the ejection fraction (EF). After gestation, amiodarone was reinitiated and switched to flecainide after implantation of a subcutaneous defibrillator as a safety net. At follow-up, LV function had almost normalized. Genetic analysis confirmed an SCN5A mutation. Discussion: Multifocal ectopic Purkinje-related premature contractions syndrome is associated with SCN5A mutation which in our case (R222Q) is the most common described. Flecainide can be an appropriate treatment option when ablation is ineffective. Defibrillator—even a subcutaneous type—could be implanted in cases of LV dysfunction or scar. PVCs suppression by flecainide and restoration of EF implies an arrhythmia—induced mechanism of LV impairment.

Coronary microvascular disease (CMVD) is not an uncommon complication after acute myocardial infarction (AMI), independent of prompt revascularization. It is a serious yet underdiagnosed disease that has a major impact on patient outcomes. Even when the infarct-related artery is successfully revascularized, a significant percentage of patients still have compromised microvascular circulation, which is linked to higher cardiovascular mortality and hospitalization for heart failure. The well-known invasive methods, such as the index of microvascular resistance (IMR) and the coronary flow reserve (CFR), have been considered as gold standards. However, they are constrained by their hazards and complexity. Non-invasive techniques, such as echocardiography Doppler for CFR assessment, positron emission tomography (PET), cardiac magnetic resonance imaging (CMR), and some other techniques provide alternatives, but their accessibility, cost and implementation during the peri-AMI period raise obstacles to their wider use. This review highlights both invasive and non-invasive modalities as it examines the diagnostic methods and prognostic significance of CMVD development early after AMI. Enhancing long-term results in this high-risk population requires a thorough understanding of pathophysiology and a commitment to larger diagnostic and prognostic studies for CMVD.

Aortic valve stenosis (AS) is a prevalent and progressive valvular disease that poses significant diagnostic challenges, particularly in low-flow, low-gradient (LF-LG) states. Accurate assessment of AS severity is crucial for timely intervention and improved clinical outcomes. This narrative review critically evaluates the limitations of conventional echocardiographic techniques and explores the role of multimodal imaging—including advanced echocardiography, computed tomography (CT), and cardiac magnetic resonance (CMR)—in enhancing diagnostic accuracy. Special emphasis is placed on the unique challenges of LF-LG AS, where standard Doppler-derived assessments may misclassify disease severity, necessitating a more integrative diagnostic approach. By addressing these key diagnostic uncertainties and proposing a multimodal framework for improved assessment, this review provides a comprehensive update on best practices in AS evaluation, with the goal of optimizing clinical decision making and patient outcomes.

In patients with radial artery occlusion (RAO), contralateral transradial access (TRA) may be infeasible or strategically undesirable. Transulnar access (TUA) ipsilateral to RAO is anatomically plausible; however, contemporary evidence on vascular safety and hand function is limited and methodologically heterogeneous. ULNART is a prospective, multicenter cohort designed to evaluate the short- and long-term safety and functional outcomes of TUA ipsilateral to RAO using standardized imaging, quantitative testing, and patient-reported outcome measures (PROMs). Adults with documented RAO undergoing elective invasive coronary angiography or percutaneous coronary intervention (PCI) are enrolled when contralateral TRA is not feasible or when preservation of the contralateral radial artery is clinically desirable. Baseline assessment includes color duplex ultrasonography (CDUS) to confirm RAO and evaluate ulnar artery suitability. A focused bilateral neurologic examination in the ulnar nerve distribution is performed to identify pre-existing motor or sensory deficits. Bilateral quantitative assessment of hand function and sensation includes handgrip strength, key pinch strength, and tactile thresholds, measured using validated instruments (JAMAR dynamometer, pinch gauge, and WEST monofilaments). Patient-reported outcomes are collected using the Quick Disabilities of the Arm, Shoulder and Hand (QuickDASH) and Cold Intolerance Symptom Severity (CISS) questionnaires. Procedures are performed via TUA ipsilateral to RAO with per-protocol anticoagulation and hemostasis is achieved with a compression device adapted at the access-site point. Patent hemostasis is initially confirmed by CDUS and then monitored by plethysmography on the fifth digit. Follow-up assessments, including CDUS, neurologic examination, and bilateral functional testing, are conducted within 24 h after hemostatic band removal and at 30 and 180 days. The primary endpoint is a composite of serious access-related vascular and clinical neuromuscular complications at 30 days. Secondary endpoints include access-site crossover rate, early (≤24 h) and delayed (6-month) access-related complications, and longitudinal changes in handgrip strength, key pinch strength, tactile sensibility, and PROMs. The study targets 127 participants, providing a two-sided 95% confidence interval with a ± 4% half-width around an expected 5% primary event rate. ULNART will provide prospective evidence on the safety of TUA ipsilateral to RAO and its effect on hand function. The findings are intended to guide access selection when TRA is unavailable, inform patient counseling, and support follow-up strategies in this population.