Up to 4 million patients with signs of myocardial ischemia have no obstructive coronary artery disease (CAD). The absence of precise guidelines for diagnosis and treatment in non-obstructive CAD encourages the scientific community to fill the gap knowledge, to provide non-invasive and less expensive diagnostic tools. The aim of our study was to explore the biological profile of Ischemia with Non-Obstructive Coronary Arteries (INOCA) patients with microvascular dysfunction compared to patients presenting with obstructive chronic coronary syndrome (ObCCS) in order to find specific hallmarks of each clinical condition. We performed a gene expression array from peripheral blood mononuclear cells (PBMCs) isolated from INOCA (n = 18) and ObCCS (n = 20) patients. Our results showed a significantly reduced gene expression of molecules involved in cell adhesion, signaling, vascular motion, and inflammation in INOCA as compared to the ObCCS group. In detail, we found lower expression of Platelet and Endothelial Cell Adhesion Molecule 1 (CD31, p < 0.0001), Intercellular Adhesion Molecule-1 (ICAM1, p = 0.0004), Tumor Necrosis Factor (TNF p = 0.0003), Transferrin Receptor (TFRC, p = 0.002), and Vascular Endothelial Growth Factor A (VEGFA, p = 0.0006) in the INOCA group compared with ObCCS. Meanwhile, we observed an increased expression of Hyaluronidase (HYAL2, p < 0.0001) in INOCA patients in comparison to ObCCS. The distinct expression of molecular biomarkers might allow an early and non-invasive differential diagnosis between ObCCS and INOCA, improving clinical management and treatment options, in the era of personalized medicine.

Aims: How the underlying aetiology and pathophysiology of left ventricular (LV) hypertrophy affects left atrial (LA) remodelling and function remains unexplored. The present study aims to investigate the influence of various hypertrophic phenotypes on LA remodelling and function. Methods and results: Patients with LV hypertrophy who underwent cardiac magnetic resonance (CMR) were compared to a control group. CMR data were analysed retrospectively to assess LA strain, volume, sphericity, and left atrioventricular coupling index (LACI). Independent clinical associates of LA strain were assessed using multivariable linear regression analysis. A total of 375 individuals were included: 148 with hypertrophic cardiomyopathy (HCM), 35 with cardiac amyloidosis (CA), 41 with hypertensive (HTN) heart disease, 97 with severe asymptomatic aortic stenosis (AS), and 54 with normal CMR. Indexed LA end-systolic (iLVmax), diastolic volumes, and LA sphericity were the largest in patients with CA (59.1 ± 16.9 mL/m2, 46.8 ± 16.4 mL/m2, and 83.2 ± 2.1%, respectively). Patients with CA presented a higher LACI when compared with other groups (58 ± 2% vs. 42 ± 2% in HCM, 39 ± 2% in HTN heart disease, 37 ± 2% in AS, and 22 ± 1% in normal), while no differences were observed across others. Patients with CA showed the lowest LA reservoir [9.6% (0.6–18.6%)] and booster strain (9.1 ± 5.4%), whereas no differences were observed across other groups. LACI and iLAVmax were independently correlated with LA reservoir (β = 0.15 and β = −39.33, respectively), LA conduit (β = 0.08 and β = −17.08, respectively), and LA booster strains (β = 0.1 and β = −28.69, respectively). LA sphericity was independently correlated with LA reservoir strain (β = −0.51). Finally, LV global longitudinal strain was independently correlated with LA reservoir (β = −0.43), conduit (β = −0.20), and booster strain (β = −0.24). Conclusion: LA characteristics differ among LV hypertrophic phenotypes. LACI and iLAVmax are independently correlated with LA function, while LA sphericity correlates independently with LA reservoir strain.

Cristina Conte, MD, Cristina Campoamor Cela, Victoria Delgado, MD, PhD, Elena Ferrer-Sistach, MD, PhD; Atrial functional mitral regurgitation: the tip of the ic

Background: Epicardial mapping and ablation of ventricular tachycardia (VT) are used in different clinical situations but pericardial adhesions following prior cardiac surgery or previous epicardial procedures may limit a percutaneous approach. The objective of this case series is to evaluate the safety and feasibility of a hybrid approach with surgical epicardial access as a valid alternative when pericardial space is not accessible percutaneously. Methods: After a complete preprocedural evaluation, four patients with prior cardiac surgery underwent hybrid VT ablation under general anesthesia. Surgical subxiphoid access was performed in three cases and one patient was subjected to median resternotomy for concomitant open-heart surgery. Epicardial electroanatomic voltage maps were acquired using the CARTO 3 system (Biosense Webster) or NavX (St. Jude Medical) and VT ablations with irrigated catheters were performed. The procedural endpoint was VT non-inducibility and/or LAVA/LP abolition. Results: No serious periprocedural complications occurred after hybrid VT ablation. Three patients had no complex ventricular arrhythmias after a median follow-up of 43 months. A symptomatic sustained VT relapsed in one patient, without requiring a redo ablation procedure but responded to escalation of antiarrhythmic therapy. Conclusions: A carefully planned hybrid VT ablation with surgical epicardial access is a safe and feasible procedure in patients with epicardial scar-related re-entry circuits and pericardial adhesions that limit a percutaneous approach.

Mariana Martino, MD, Cristina Conte, MD, Elena Ferrer-Sistach, MD, PhD, Victoria Vilalta, MD, PhD, Victoria Delgado, MD, PhD; Transcatheter intervention in mass