Three-dimensional TEE is more accurate than 2DTTE and 2DTEE for determining LVOT and AA dimensions. When AS severity is determined by 3DTEE and corrected for PR using the 3D values, it needs to be reclassified from severe to moderate in almost a third of patients.

Despite the introduction of drug-eluting stents to combat the neointimal hyperplasia that occurred after BMS implantation, in-stent restenosis is still encountered in a significant number of patients, particularly as increasingly complex lesions are tackled by percutaneous coronary intervention. Many biological and mechanical factors interplay to produce restenosis, some of which are avoidable. Intravascular imaging provided unique insights into various forms of stent-related mechanical issues that contribute to this phenomenon. From a practical perspective, intravascular imaging can therefore help to optimize the stenting procedure to avert these issues. Moreover, once the problem of restenosis eventuates, imaging can guide the management by tackling the underlying identified mechanism. Finally, it can be used to evaluate the re-intervention results. Nevertheless, with the emergence of different treatment options, more evidence is needed to define patient/lesion-specific characteristics that may help to tailor treatment selection in a way that improves clinical outcomes.

No abstract

Many patients who present with symptoms or objective evidence of ischemia have no or non-physiologically-significant disease on invasive coronary angiography. The diagnosis of ischemic heart disease is thus often dismissed, and patients receive false reassurance or other diagnoses are pursued. We now know that a significant proportion of these patients have coronary microvascular dysfunction and/or vasospastic disease as the underlying pathophysiology of their clinical presentation. Making the correct diagnosis of such abnormalities is important not only because they impact the quality of life, with recurring symptoms and unnecessary repeated testing, but also because they increase the risk for adverse cardiovascular events. The mainstay of diagnosis remains an invasive comprehensive physiologic assessment, which further allows stratifying these patients into appropriate “endotypes”. It has been shown that tailoring treatment to the patient’s assigned endotype improves symptoms and quality of life. In addition to the conventional drugs used in chronic stable angina, multiple newer agents are being investigated. Moreover, innovative non-pharmacologic and interventional therapies are emerging to provide a bail-out in refractory cases. Many of these novel therapies fail to show consistent benefits, but others show quite promising results.

Background: Bacterial infections are a frequent cause of acute morbidity and sometimes mortality in sickle cell disease (SCD). Splenic dysfunction alone does not explain the susceptibility to specific organisms e.g., Staphylococcus aureus and Klebsiella as shown in some studies; suggesting that the splenic dysfunction is not the only explanation and that neutrophil dysfunction may be present. Neutrophils destroy microbes by producing a burst of reactive oxygen species (ROS) (respiratory burst) in response to bacterial components, as well as to phorbol-myristate-acetate (PMA). Some studies have shown that the state of chronic hemolysis in SCD impairs the ability to develop neutrophils to mount a bactericidal oxidative burst, and hence increasing susceptibility to bacterial infections. Aims: to assess the neutrophil oxidative burst in SCD patients and explore the relation to markers of hemolysis. Methods: Twenty-seven hydroxyurea naïve children and adolescents with SCD (mean age 11.1 ± 3.9 years) were enrolled from Pediatric Hematology Clinic at Ain Shams University Children's Hospital. They were compared to 26 age-and sex-matched healthy controls. Patients were studied stressing on transfusion history, chelation therapy, serum ferritin, hematological profile, markers of hemolysis and serum haptoglobin. Neutrophil oxidative burst assay was performed using DHR based flow cytometry. Results: Eleven (40%) out of the 27 patients had HBSS while 16 (60%) patients were sickle thalassemias. Six patients (22.2%) were splenectomized. Severe vaso-occlusive crisis and acute chest syndrome were found in 22.2% and 18.5% of patients, respectively. Four (14.8%) patients had evidence of stroke. Bone fractures and avascular necrosis were found in 5.5% and 11.1 % of patients, respectively. Most of the studied patients were on chelation therapy, either as monotherapy or combined chelation (37% each). White blood cell count and reticulocytic count were significantly higher in SCD patients as compared to healthy controls (P = 0.03 and <0.01 respectively).