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Cardiac CT-Scan and cardiac magnetic resonance imaging (MRI) are two booming cardiac imaging modalities especially in chest pain screening for CT-Scan and in surveillance of patients with known coronary artery disease for MRI. Artificial Intelligence is already of great help in radiologic diagnosis and its use should widen in the next few years. Teleradiology allows remote interpretation of all radiology exams and should develop in cardiac imaging. Expert radiology diagnosis centers should develop gathering cardiologists and radiologists with great experience in the field of cardiac imaging interpretation. Peripheral acquisition radiology centers would be disseminated all across the country without a need for a local expert and would send their images to the expert center for interpretation. The expert center would be the middle of this spider web, sending back the report and the selected images to the peripheral center, allowing optimal care for all patients nationwide. Artificial Intelligence would be a major asset of these expert centers, improving through the years. This operating mode would allow the onset of systematic screening for coronary artery disease in the global population and the surveillance of known coronary artery disease treated patients.

The etiology of cardiac masses is often oncological or thrombotic, rarely inflammatory. Among heart tumors, the vast majority are metastatic. We describe the most frequent benign primary cardiac tumors and the most frequent malignant primary cardiac tumors and give information about the advantages of using a multi-modality approach for the accurate diagnosis of a cardiac mass using Computed Tomography Scanner and Magnetic Resonance Investigation.

Infiltrative cardiomyopathies are abnormal accumulations or depositions of different substances in cardiac tissue leading to its dysfunction, first diastolic, then systolic. The different infiltrative cardiomyopathies are amyloidosis (both light chain amyloidosis and transthyretin amyloidosis variants), lysosomal and glycogen storage disorders (Fabry-Anderson disease), and iron overload (hemochromatosis and thalassemia associated with blood transfusions), as well as inflammatory diseases such as sarcoidosis. We also evoke hypereosinophilic syndrome associated with endomyocardial fibrosis. Echocardiography is the first essential step after interrogatory and clinical examination and may help the cardiologist as a screening tool. Cardiac MRI is the second fundamental step towards the diagnosis especially due to the late gadolinium enhancement and to the T1-mapping. Cardiac amyloidosis diagnosis also requires the use of nuclear imaging. Cardiac CT-Scan may be useful for estimating the amyloid load, identify potential cardiac thrombus and rule out associated coronaropathy.

Atherosclerosis is one of the two major causes of mortality worldwide along with cancer and is responsible for myocardial infarction, stroke, and arteritis. Its pathophysiology is still partially understood which allows doubts referring to the preventive and curative treatments. Population screening for atherosclerosis remains marginal even though it should be the common practice. To encourage preventive screening and therapies, we propose a simple and easily understandable pathophysiology of atherosclerosis, explaining how the brick-wall of atheroma is build inside the intima of arteries using a metaphor: the LDL-cholesterol bricks, the oxidation cement, and the inflammatory mason.

Cardiac CT-Scan and cardiac magnetic resonance imaging (MRI) are two booming cardiac imaging modalities especially in chest pain screening for CT-Scan and in surveillance of patients with known coronary artery disease for MRI. Artificial Intelligence is already of great help in radiologic diagnosis and its use should widen in the next few years. Teleradiology allows remote interpretation of all radiology exams and should develop in cardiac imaging. Expert radiology diagnosis centers should develop gathering cardiologists and radiologists with great experience in the field of cardiac imaging interpretation. Peripheral acquisition radiology centers would be disseminated all across the country without a need for a local expert and would send their images to the expert center for interpretation. The expert center would be the middle of this spider web, sending back the report and the selected images to the peripheral center, allowing optimal care for all patients nationwide. Artificial Intelligence would be a major asset of these expert centers, improving through the years. This operating mode would allow the onset of systematic screening for coronary artery disease in the global population and the surveillance of known coronary artery disease treated patients.

Circulatory failure following cardiac arrest (CA) requires catecholamine support and occasionally veno-arterial extracorporeal membrane oxygenation (vaECMO). VaECMO-generated blood flow is continuous and retrograde, increasing ventricular stroke work. Our aim was to assess the benefit of a device generating a pulsatile vaECMO flow synchronized with the heart rhythm lowering systolic vaECMO output on the left ventricular ejection fraction (LVEF) and pulmonary capillary pressure (Pcap) after CA. This experimental randomized study in pigs compared standard nonpulsatile vaECMO (control) with pulsatile synchronized vaECMO (study) group using a pulsatility-generating device. After sedation and intubation, ventricular fibrillation was induced by pacing. After 10-min ventricular fibrillation, cardiopulmonary resuscitation was performed for 20 min then vaECMO, defibrillation and 0.15 µg/kg/min intravenous epinephrine infusion were initiated. Hemodynamics, Pcap, LVEF by echocardiography and angiography were measured at baseline and every 30 min after the vaECMO start until vaECMO and epinephrine were stopped (at 120 min), and 30 min later. Baseline hemodynamics did not differ between groups; 120 min after vaECMO initiation, LVEF by echocardiography and angiography was significantly higher in the study than control group 55 ± 19% versus 34 ± 13% (P = 0.042), 50 ± 16% versus 33 ± 12% (P = 0.043), respectively. Pcap decreased from baseline by 4.2 ± 8.6 mm Hg in the study group but increased by 5.6 ± 5.9 mm Hg in the control group (P = 0.043). Thirty minutes later, LVEF remained higher in the study group 44 ± 7% versus 26 ± 11% (P = 0.008) while Pcap did not differ. A synchronized pulsatile device decreasing systolic output from vaECMO improved LVEF and Pcap in a pig model of CA and resuscitation.

Clinical trials of cell therapy in stroke favor autologous cell transplantation. To date, feasibility studies have used bone marrow-derived mononuclear cells, but harvesting bone marrow cells is invasive thus complicating bedside treatment. We investigated the therapeutic potential of peripheral blood-derived mononuclear cells (PB-MNC) harvested from diabetic patients and stimulated by ephrin-B2 (PB-MNC+) (500,000 cells), injected intravenously 18–24 hours after induced cerebral ischemia in mice. Infarct volume, neurological deficit, neurogenesis, angiogenesis, and inflammation were investigated as were the potential mechanisms of PB-MNC+ cells in poststroke neurorepair. At D3, infarct volume was reduced by 60% and 49% compared to unstimulated PB-MNC and PBS-treated mice, respectively. Compared to PBS, injection of PB-MNC+ increased cell proliferation in the peri-infarct area and the subventricular zone, decreased microglia/macrophage cell density, and upregulated TGF-βexpression. At D14, microvessel density was decreased and functional recovery was enhanced compared to PBS-treated mice, whereas plasma levels of BDNF, a major regulator of neuroplasticity, were increased in mice treated with PB-MNC+ compared to the other two groups. Cell transcriptional analysis showed that ephrin-B2 induced phenotype switching of PB-MNC by upregulating genes controlling cell proliferation, inflammation, and angiogenesis, as confirmed by adhesion and Matrigel assays.Conclusions. This feasibility study suggests that PB-MNC+ transplantation poststroke could be a promising approach but warrants further investigation. If confirmed, this rapid, noninvasive bedside cell therapy strategy could be applied to stroke patients at the acute phase.

BACKGROUND In treated hypertensives, extreme-dippers with stable coronary artery disease (CAD) exhibit more severe nighttime cardiac ischemia than dippers. After excluding confounding factors such as diabetes, CAD or chronic kidney disease (CKD), we assessed whether subendocardial viability, determined by the Buckberg index, was more significantly impaired in extreme-dippers than in dippers. METHODS Two hundred thirteen consecutive treated hypertensives (156 dippers, 57 extreme-dippers), were included. After 24-hour ambulatory blood pressure (BP) monitoring, patients underwent radial applanation tonometry (with determination of: subendocardial viability ratio [SEVR], central augmentation index [AIx], and pulse pressure amplification [PPamp]), carotid-femoral pulse wave velocity (cfPWV) measurement, and cycle ergometer stress testing. RESULTS Extreme-dippers showed higher cfPWV (8.99 ± 2.16 vs. 8.29 ± 1.69 m/s, P = 0.014), higher AIx (29.7 ± 9.4 vs. 26.4 ± 10.4%, P = 0.042), lower PPamp (1.22 ± 0.14 vs. 1.30 ± 0.15, P < 0.001), lower SEVR (146 ± 23% vs. 157 ± 26%, P = 0.007), and lower nighttime diastolic BP (DBP) (70 ± 9 vs. 75 ± 9 mm Hg, P < 0.001) than dippers. SEVR and cfPWV were inversely correlated. Among extreme-dippers, women exhibited lower SEVR (138 ± 21% vs. 161 ± 23%, P = 0.004), PPamp (1.16 ± 0.10 vs. 1.31 ± 0.15, P < 0.001), and nighttime DBP (67 ± 8 mm Hg vs. 72 ± 8 mm Hg, P = 0.017) than men. CONCLUSIONS Extreme-dipper treated hypertensives with no history of CAD, diabetes or CKD, present increased aortic stiffness and low PPamp. Furthermore, this is the first demonstration of the greater likelihood of these patients to exhibit impaired subendocardial viability compared to dippers. Extreme-dipper hypertensive patients, women in particular, may have a significantly higher risk of silent myocardial ischemia, thus justifying systematic screening.

Coronary artery aneurysm may cause coronary artery rupture, thromboembolism or haemodynamic problems related to compression. We report the case of a 68-year old man who was referred to an intensive cardiological care unit for recurrence of ventricular tachycardia. Coronary angiography revealed two large aneurysms of the mid-right coronary artery. A multislice computed tomography (CT) study demonstrated marked underestimation by invasive angiography because of the large thrombus. The patient was referred for cardiac surgery. The right mammary artery was used as a bypass graft to the distal segment of the right coronary artery and the two aneurysms were ligated proximally and distally after removal of their thrombus filling. The postoperative CT confirmed patency of the bypass graft and the vascular exclusion of the aneurysm, with no opacification. Cardiac CT is a promising tool for the comprehensive study of coronary aneurysms, both before and after surgery.

Introduction: Hepatocellular carcinoma (HCC) is the second cause of cancer-related deaths worldwide. While sorafenib may improve overall survival in advanced HCC, new therapies are needed. Both preclinical and clinical data support a role of MET and AXL receptor tyrosine kinases in HCC progression. We thus evaluated S49076, a novel MET/AXL/FGFR inhibitor in HCC cell lines in vitro and in a transgenic mouse model of HCC. Materials and Methods: MET and AXL expressions were assessed in a panel of HCC cell lines by western blot. Downstream signaling pathways were investigated in the presence of HGF, GAS6 and S49076. Cell invasion was evaluated on matrigel assay. Transgenic mice developing stage-defined HCC were treated with S49076 (50mg/kg). Tumor response was evaluated measuring liver volume by echo-doppler and the number of tumor nodules at intermediary (12weeks) and final sacrifice (16 weeks). Results: Both MET and AXL are expressed in the majority of HCC lines screened. Notably, a high level of AXL was observed in the SK-HEP1 cells which were therefore selected for further investigation. MET and AXL pathways were strongly stimulated by their respective ligands, HGF and GAS6. Combination of HGF and GAS6 led to marked activation of ERK. S49076 inhibited MET and AXL pathway activation and HGF- and GAS6- induced invasion at nanomolar concentrations. In vivo anti-tumor efficacy of S49076 was demonstrated in a transgenic MET-expressing mouse model of HCC. Conclusion: S49076 displayed strong MET and AXL pathway inhibition and anti-invasive properties in SK-HEP1 HCC cells. Moreover, S49076 demonstrated antitumor activity in a mouse model of HCC. Together, these results would support development of S49076 as an innovative treatment in HCC patients. Citation Format: Annemilai Tijeras-Raballand, Adrien Pasteur-Rousseau, Matthieu Martinet, Philippe Bonnin, Marc Pocard, Sébastien Banquet, Valérie Cattan, Eric Raymond, Armand de Gramont. S49076, a novel kinase inhibitor of MET, AXL and FGFR, demonstrates marked in vitro and in vivo efficacy in hepatocellular carcinoma. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 321.