Feasibility and safety of cryoballoon ablation for atrial fibrillation and closing patent foramen ovale without implantation：A pilot study.

BACKGROUND: Patent foramen ovale (PFO) affects 20%-34% of adults and is associated with strokes and other disorders. The conventional treatment of PFO-related strokes is a closure procedure. The metal device is associated with some adverse events. OBJECTIVE: Our aim was to investigate the efficacy and safety of PFO closure using cryoablation without implantation in patients with atrial fibrillation (AF) who underwent pulmonary vein isolation (PVI). METHODS: We divided the 22 patients with both PFO and AF who underwent PVI via cryoablation into 2 groups: standard PVI + atrial septum (AS) cryoablation group (group 1, n = 11) and standard PVI group (group 2, n = 11). The guidewire accesses the left atrium through the PFO without AS puncture during the procedure. Standard PVI via cryoablation was performed. The cryoballoon was retracted to the right atrium and inflated against the AS post-PVI. Patients in group 1 had cryoablation for 120-150 seconds, whereas patients in group 2 received sham ablation. The co-primary end points were the PFO closure rate and a composite of AF recurrence and stroke/transient ischemic attack (TIA) events. RESULTS: There were no differences in procedure-related adverse events between the 2 groups. Neither group had an ischemic stroke report at 1-year follow-up. The PFO closure rate at 6 months in group 1 was significantly higher than that in group 2 (7 [63.6%] vs 1 [9.1%]; P = .002). AF recurrence after ablation was comparable in both groups at 3 months (3 [27.3%] vs 1 [9.1%]; P = .269), 6 months (0 vs 0), and 12 months (2 [18.2%%] vs 1 [9.1%]; P = .534) of follow-up. CONCLUSION: Cryoablation is a safe and effective approach to close PFO in patients with AF undergoing PVI in a single procedure.

Site of left axillary vein crossing the clavicle: an analysis with computed tomography venography as a guide for vein puncture for device implantation.

BACKGROUND: Blind axillary venous access is a convenient but technically difficult approach for cardiac rhythm device lead implantation. We try to explore whether there are rules on the axillary vein course to facilitate blind venous cannulation. METHODS: In a single-center, retrospective study, we included 155 patients who underwent computed tomography venography (CTV) examination of left axillary vein. All scans were reviewed for the relationship between left axillary vein and clavicle, vein steepness, and depth. Factors probably affecting above indicators were analyzed. RESULTS: The location of left axillary vein crossing the clavicle was mainly concentrated around the medial 1/3 of clavicle, with mean crossing location of the medial 1/3 of clavicle, which was not correlated with sex, age, abdominal subcutaneous fat thickness, upper thoracic kyphosis angle, or the angle between clavicle and anterior midline (P < 0.05). The average angle between axillary vein and horizontal line was 31.57 ± 11.72°, which was positively associated with age, whereas inversely associated with the angle between clavicle and anterior midline (P < 0.05). The proximal axillary vein ran more and more shallow until becoming the subclavian vein (P < 0.01); and it had a mean depth of 3 cm, which was significantly associated with abdominal subcutaneous fat thickness (P < 0.05). CONCLUSIONS: The left axillary vein and clavicle had a relatively fixed relationship that axillary vein commonly crossed the medial 1/3 of clavicle. The average angle between axillary vein and horizontal line was 31.57 ± 11.72°, associated with age and the clavicle course. The mean depth of proximal axillary vein was 3 cm, and patients with larger weight had a deeper position of axillary vein.

Novel dry pericardiocentesis: Transvenous puncture of the right ventricle with the back end of a 0.014-inch PTCA guidewire and a 1.8 Fr microcatheter.

Background: Dry transthoracic pericardiocentesis is challenging and carries the risk of right ventricle (RV) or coronary artery injury. The RV can usually control bleeding automatically. For example, most perforations of the RV caused by pacemaker leads are treated without open surgery. Thus, we performed a transvenous puncture of the RV for dry pericardiocentesis with the back end of a 0.014-inch percutaneous transluminal coronary angioplasty (PTCA) guidewire and a 1.8 Fr microcatheter. Methods: The back end of a 0.014-inch PTCA guidewire within a 1.8 Fr microcatheter was used to transvenously punctured through the middle of the acute margin of the RV into the pericardial space in 12 Yorkshire swine and 5 beagles. PTCA balloons of different diameters were used to dilate the puncture holes for 15 min under anticoagulation in all the animals to assess the ability of the RV to control the bleeding. Then, for 3 days, the puncture hole was dilated by a 6 Fr catheter in 9 swine and 5 dogs. Results: The puncture was successful in all the animals. After withdrawal of the 2.5-mm balloon or the 6 Fr catheter, none of the animals exhibited pericardial effusion, as observed by echocardiography. There was no sustained ventricular arrhythmia or other complications. All the animals survived. Conclusion: Transvenous puncture of the right ventricle with the back end of a 0.014-inch PTCA guidewire and 1.8 Fr microcatheter may be feasible and have a good safety margin.

Acute Myocardial Infarction Followed by Cerebral Hemorrhagic Infarction in Polycythemia Vera: Case Report and Literature Review.

A 60-year-old man presented to our emergency room with severe chest pain. Based on the electrocardiogram and elevated serum troponin T levels, acute coronary syndrome was suspected. Coronary angiography revealed total occlusion of the middle of the left anterior descending coronary artery. However, blood cell count abnormalities were not of concern. Twelve days later, the patient developed hemorrhagic infarction in the right parieto-occipital lobe. Acute coronary syndrome and cerebral hemorrhagic infarction were primarily caused by thrombus formation due to polycythemia vera (PV), based on the presence of increased blood consistency on admission. PV was diagnosed after bone marrow biopsy and genetic testing. The patient was treated with descending cell and antiplatelet therapy. Our case highlights the importance of the urgent identification of PV. When acute myocardial infarction occurs in patients with no significant risk factors for cardiovascular disease, blood routine abnormalities should be paid close attention to. If PV was diagnosed as early as possible, thrombotic and hemorrhagic complications could be prevented in the early stages.

A functional variant of the long noncoding RNA AL110200 is associated with the risk of ischaemic stroke recurrence.

BACKGROUND AND PURPOSE: This study aimed to test the hypothesis that long noncoding RNA (lncRNA) AL110200 exerts a proinflammatory effect on atherosclerosis and that the variant rs901681 contributes to ischaemic stroke incidence and recurrence. METHODS: The expression of AL110200 was analyzed in THP-1 cells treated with oxidized low-density lipoprotein and in human peripheral blood in a coronary heart disease and control population to determine the role of AL110200 in atherosclerosis. The effect of AL110200 on cell adhesion and invasion was tested. The plasma level of leukotriene B4 and rs901681 genotype distribution were assessed in 220 participants. In 1004 ischaemic stroke patients and 1434 controls, the association between rs901681 and stroke incidence was analyzed by logistic regression, and the association of rs901681 and stroke prognosis was analyzed using Kaplan-Meier analysis and the Cox proportional hazards model. RESULTS: Increased expression of AL110200 was observed in THP-1 cells under oxidized low-density lipoprotein treatment. Knockdown of AL110200 reduced the adhesive and invasive ability of THP-1 cells. AL110200 expression in peripheral blood was significantly higher in the coronary heart disease group than in the controls. The GG genotype of rs901681 is associated with reduced plasma leukotriene B4. In the ischaemic stroke population, rs901681 was not associated with ischaemic stroke incidence (p = 0.686). Patients carrying rs901681 GG had a lower risk for stroke recurrence at age ≥60 years (p = 0.001), cardiovascular stroke death (p = 0.022) and all-cause mortality (p = 0.034) in the all-age group. CONCLUSIONS: AL110200 might exert a proinflammatory effect on atherosclerosis, and the variant rs901681 might be a strong predictor of stroke prognosis in ischaemic stroke patients.

A non-invasive method to assess cerebral perfusion pressure in geriatric patients with suspected cerebrovascular disease.

BACKGROUND: Cerebral perfusion pressure (CPP) can adversely impact cerebrovascular hemodynamics but cannot be practically measured in most clinical settings. Here, we aimed to establish a representative mathematical model for CPP in geriatric patients with suspected cerebrovascular disease. METHODS: A total of 100 patients (54 males and 46 females between 60-80 years of age) with suspected cerebrovascular disease and no obvious cerebrovascular stenosis were selected for invasive CPP monitoring via catheterization of the middle segment of the common carotid arteries and openings of the vertebral arteries bilaterally. Curves were function-fitted using MATLAB 7.0, and data was statistically processed by SPSS 20.0. RESULTS: MATLAB 7.0 constructed eighth-order Fourier functions that fit all recorded CPP curves. Since the coefficients of the 100 functions were significantly different, all functions were standardized to derive one representative function. By manipulating the heart rate and maximum/minimum CPP of the representative function, estimated CPP curves can be constructed for patients with differing heart rates, intracranial pressures (ICPs) and blood pressures. CONCLUSIONS: CPP can be well-modeled through an eighth-order Fourier function that can be constructed from a patient's brachial artery blood pressure (BABP), ICP and heart rate. This function is representative of geriatric patients with cerebrovascular disease and can be used in the future study of cerebral hemodynamics.

Hypercholesterolemia increases the production of leukotriene B4 in neutrophils by enhancing the nuclear localization of 5-lipoxygenase.

AIMS: Neutrophils can synthesize leukotriene B4 (LTB4) by activating the 5-lipoxygenase (5-LO)signaling pathway. LTB4 is a pro-inflammatory mediator associated with the etiology and progression of atherosclerosis. It can increase function and number of neutrophils in an autocrine manner. Since hypercholesterolemia is associated with an increase in the number and function of neutrophils, we hypothesized that this effect could be mediated through increased production of LTB4 in neutrophils. METHODS/RESULTS: Hypercholesterolemia was modeled in Wistar rats by feeding them with a high cholesterol diet. The induction of hypercholesterolemia caused an increase in the plasma levels of LTB4, following lipopolysaccharide stimulation. This effect was recapitulated in vitro, both in the presence and absence of stimulation with the activator of 5-LO, A23187. Neutrophils in hypercholesterolemia rats expressed similar total levels of 5-LO as control rats, but displayed increased nuclear localization of 5-LO, as well as elevated levels of phosphorylated 5-LO and ERK1/2. In vitro, MßCD/cholesterol complexes enriched cholesterol in neutrophils, resulted in similar changes in 5-LO/LTB4. In addition, these alterations could be inhibited with the ERK inhibitor PD98059. CONCLUSION: Hypercholesterolemia increases LTB4 production in neutrophils by increasing the nuclear localization of 5-LO, which is the result of its phosphorylation by activated ERK1/2.

In atherogenesis, the apoptosis of endothelial cell itself could directly induce over-proliferation of smooth muscle cells.

Over-proliferation of SMC (smooth muscle cell) is one characteristics of atherosclerosis. One well accepted mechanism is that the decrease of ECs (endothelial cells) induced by over apoptosis leads to endothelial dysfunction, which in turn results in over-proliferation of SMC. Obviously, the mechanism works after endothelial apoptosis. Compared with necrosis, apoptosis is time and energy consuming. The question is why the cell ends in the form of apoptosis instead of necrosis. From the evolutionary standpoint, apoptosis has some useful functions other than removing the damaged or unwanted cells. Recent studies showed that cells nearby the apoptotic ones began to proliferate and differentiate before apoptosis and the apoptotic signals could induce the near cells to proliferate without the death of cells. Apparently, some mechanism in apoptosis results in the proliferation of cells. So, we hypotheses that endothelial apoptosis can directly induce the over-proliferation of SMC.