Background: Atherosclerosis increases the risk of acute-phase CI (aCI) and acute myocardial infarction (AMI), which can be life threatening. Atherosclerosis is also closely related to diabetes mellitus (DM) and chronic kidney disease (CKD). Novel biomarkers are needed to follow the progress of atherosclerosis.

Methods and Results: Screening by protein arrays identified deoxyhypusine synthase (DHPS) as an antigen recognized by IgG antibodies in sera of patients with both atherosclerosis and aCI and the antibody was detected in Western blots. The serum antibody levels in healthy donors (HDs) and patients with aCI, transient ischemic attack (TIA), DM, AMI, or CKD were determined by enzyme-linked immunosorbent assay (ELISA) and amplified luminescent proximity homogeneous assay (Alpha) LISA using recombinant DHPS protein. Serum DHPS antibody levels were significantly higher in patients with any of these diseases than in HDs. The difference was greatest in patients with DM and CKD. DHPS antibody levels were well correlated with artery stenosis and the presence of hypertension. The serum level of this DHPS antibody may reflect the extent of atherosclerosis caused by DM, CKD and/or hypertension.

Conclusions: Serum antibody levels against DHPS may be useful in diagnosing atherosclerosis and associated aCI, TIA, DM, AMI, and CVD.

Background: Antiplatelet therapy nonresponse is associated with worse clinical outcomes. The aim of this study was to investigate the association of clinical outcomes with platelet function-guided modifications in antiplatelet therapy in patients with ischemic stroke.

Methods: This is a retrospective, multicentre study. From August 2010 to December 2014, 812 patients with ischemic stroke underwent platelet function testing using platelet aggregation. Aspirin nonresponse was defined as a mean platelet aggregation ≥20% with 0.5 mM arachidonic acid and/or ≥70% with 10 μM adenosine diphosphate. Antiplatelet therapy modification was defined as any increase in antiplatelet therapy after testing. Clinical outcomes were compared between patients with and without antiplatelet therapy modifications using univariate and propensity score-adjusted analyses.

Results: Among 812 patients, 223 patients had aspirin nonresponse, 204 patients were modified in antiplatelet therapy after platelet function testing. The incidence rates of ischemic events, death, or bleeding events were not significantly different between the patients with and without antiplatelet therapy modification. However, in patients with aspirin nonresponse, antiplatelet therapy modification was associated with decreased ischemic events (hazard ratio, 0.68; 95% CI, 0.61-0.95; P = 0.01) and ischemic stroke (hazard ratio, 0.71; 95% CI, 0.64-0.99; P = 0.04) compared with no modification in antiplatelet therapy. No differences in bleeding events were observed between two groups.

Conclusions: In patients with aspirin nonresponse, platelet function-guided modification in antiplatelet therapy after an ischemic stroke was associated with significantly lower rate of ischemic events. The platelet function testing is may be useful to guide antiplatelet therapy modification.

A lady, 67 years old, 60 Kg, about 7 hours she was admitted to local hospital due to acute chest pain. She was diagnosed with acute anterior wall myocardial infarction and received thrombolysis treatment with Reteplase and loading dose of aspirin and clopidogrel following a standard dual antiplatelet therapy strategy. Her symptoms were quickly relieved and reperfused according ECG criteria. And then she was transferred to Zhengzhou University People’s Hospital about 17 hours after her chest pain. Her first ECG in our hospital still showed anterior wall acute myocardial infarction changes (Figure 1). She didn’t have histories of hypertension and diabetes. At the tenth day, echocardiography showed: LVEDd = 52 mm, EF53 %; SPECT showed ischemic necrotic change (isotope filling defect) at anterior wall and apex. She had coronary angiography at AMI 12th day and the result showed : RCA diffuse atherosclerosis without significant stenosis; LM normal; LCX normal; Middle LAD was severe diffuse stenosis around 80-90% accompanied by severe calcification which involved with first diagonal branch orifice (B2 type lesion) (Figure 2). Through communication with patient and their families, finally we decided coronary artery intervention for LAD lesion. Because of the LAD and D1 special anatomical structure, we planned to use CULOTTES technology. With right radial artery approach, 6000u common heparin (100u/ kg body weight) was given through 6F sheath side arm, verapamil 5 mg was given to prevent radial artery spasm. We selected 6 F EBU 3.5 guiding catheter (ID = 0.72), 2 BMW wires into the distal LAD and D1, 2.5 X15 B Braun balloon to pre-dilate LAD and D1, 10atmx10 seconds respectively. China-made Firebird II (Shanghai Microport, China) 3.0 X23 stent was implanted from LAD to D1, 16 atm x 10 seconds deployed the stent (Figure 3), TIMI blood flow was good. Diagnal BMW wire was inserted into the LAD from stent strut mesh. A 2.5 X15 B Braun balloon was reused to pre-dilate stent strut mesh about 10-12 atm. When we pull back first LAD BMW wire, we met very high resistance. When the BMW wire was out, we can see distal wire (opaque X-ray segment about 30 mm) left in LAD between LAD intima and the stent (distal wire fractured) (Figure 4). We concerned that the left wire could not be removed easily and had a little effect on blood flow and prognosis, so we planned to implant

Background: Traumatic Ventricular Septal Defect (VSD) is an uncommon occurrence in cases of penetrating cardiac injury with an incidence of only 1% to 5%. Most patients require cardiac surgical or percutaneous device closure to ensure survival.

Objective: We report on a patient who had transcather closure of post traumatic ventricular septal defect with the Occlutech Patent Ductus Arteriosus Occluder device.

Methods: We treated an adult patient with post-traumatic ventricular septal defects caused by stab wound with a knife. The post traumatic ventricular septal defect was closed percutaneously with the Occlutech Patent Ductus Arteriosus Occluder.

Results: Post traumatic ventricular septal defect was closed successfully percutaneously with no residual VSD on fluoroscopy and echocardiogram. Patient was discharged the following day.

Conclusion: Our experience indicate that closure of a post traumatic ventricular septal defect using the Occlutech Patent Ductus Arteriosus Occluder is feasible , safe and effective in carefully selected patients.

A 71-year-old man, that underwent Coronary Artery Bypass Graft Surgery (CABG) several years ago, was referred for an Invasive Coronary Angiography (ICA) due toretrosternal pain and dyspnea. ICA was performed via right radial access and revealed patent Left Internal Mammary Graft (LIMA) to the Left Anterior Descending Artery (LAD). The Right Internal Mammary Graft (RIMA) to the marginal artery could not be visualized despite numerous attempts. The patient subsequently underwent cardiac CT angiography (CCTA) to evaluate the RIMA origin and patency. CCTA revealed a patent RIMA originating from an aberrant right subclavian artery, which emerged from the distal portion of the aortic arch and traversed posterior behind the esophagus to reach the right upper extremity. This variant, often termedarteria lusoria, is the most common of the aortic arch anomalies, with an estimated incidence from 0.5%-1% [1]. Such aberrant course may cause a vascular ring around the trachea and esophagus [1] and symptoms range from none to nonspecific chest pain, dysphagia and dyspnea. Our case illustrates that in scenarios where arterial grafts could not be visualized by ICA, existence of alusorian artery should be suspected. CCTA should serve as the preferred method for demonstration of such vascular anomalies.