The reentry circuit of idiopathic left ventricular tachycardia (ILVT) has been demonstrated to be confined to the left posterior Purkinje network. We hypothesized that mapping and linear ablation of the left posterior fascicle (LPF) during sinus rhythm guided by non-contact mapping can effectively modify the arrhythmogenic substrate in patients with ILVT and abolish the tachycardia.Six patients with ILVT, consisting of one case in which conventional mapping failed three times, one recurrent case, one non-inducible case and three common cases, were included in the study. After a three-dimensional endocardial geometry of the left ventricle (LV) was created, the conduction system in the LV was mapped during sinus rhythm using a filter setting of 8 Hz. The His bundle area, left bundle branch, fascicles and sinus breakout point (SBO) were mapped in detail and tagged as special landmarks in the geometry. A linear lesion was placed perpendicular to the wave front propagation direction of the LPF, 1cm above the SBO. There was a small Purkinje potential preceding the ventricular activation at its starting and ending point.The mean tachycardia cycle length of ILVT in this study was 340.3+/-51.4ms. After a mean of 5.5+/-1.6 radiofrequency deliveries, the clinical tachycardias could not be induced and the 12-lead surface ECG showed right QRS axis deviation (mean 39.7+/-26.0 degrees) in all patients. The total procedure time was 160.0+/-32.2 min with fluoroscopic time of 26.0+/-6.8 min. No ILVT was inducible during control stimulation, and none recurred during a mean follow-up of 13.0+/-4.8 months.Mapping and linear ablation of the Purkinje network in LPF area guided by non-contact mapping is an effective and safe treatment of ILVT with radiofrequency energy, especially for those ILVTs which were unsuccessfully treated by conventional means or were non-inducible or non-sustained during the procedure.
Severe hypertriglyceridemia is a well-known cause of pancreatitis. Usually, there is a moderate increase in plasma triglyceride level during pregnancy. Additionally, certain pre-existing genetic traits may render a pregnant woman susceptible to development of severe hypertriglyceridemia and pancreatitis, especially in the third trimester. To elucidate the underlying mechanism of gestational hypertriglyceridemic pancreatitis, we undertook DNA mutation analysis of the lipoprotein lipase (LPL), apolipoprotein C2 (APOC2), apolipoprotein A5 (APOA5), lipase maturation factor 1 (LMF1), and glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) genes in five unrelated pregnant Chinese women with severe hypertriglyceridemia and pancreatitis. DNA sequencing showed that three out of five patients had the same homozygous variation, p.G185C, in APOA5 gene. One patient had a compound heterozygous mutation, p.A98T and p.L279V, in LPL gene. Another patient had a compound heterozygous mutation, p.A98T & p.C14F in LPL and GPIHBP1 gene, respectively. No mutations were seen in APOC2 or LMF1 genes. All patients were diagnosed with partial LPL deficiency in non-pregnant state. As revealed in our study, genetic variants appear to play an important role in the development of severe gestational hypertriglyceridemia, and, p.G185C mutation in APOA5 gene appears to be the most common variant implicated in the Chinese population. Antenatal screening for mutations in susceptible women, combined with subsequent interventions may be invaluable in the prevention of potentially life threatening gestational hypertriglyceridemia-induced pancreatitis.
The association of strictly defined metabolic healthy obese (MHO) with subclinical cardiac function was unclear. Our study aims to examine the role of MHO in subclinical cardiac dysfunction in a Chinese population.The study subjects were recruited from Danyang from 2017 to 2019. Obesity was defined by body mass index (BMI) categories (normal weight, overweight and obesity). Metabolic health was strictly defined as having neither any of the guidelines recommended metabolic syndrome components nor insulin resistance. Thus, subjects were grouped by BMI categories and metabolic health status as six groups. Preclinical systolic (global longitudinal strain [GLS]) and diastolic function were assessed by 2D speckle tracking, and transmitral and tissue Doppler imaging, respectively. The 2757 participants (mean age ± standard deviation, 52.7 ± 11.7 years) included 1613 (58.5%) women, 999 (36.2%) obese, 2080 (75.4%) metabolically unhealthy and 93 (3.4%) MHO participants. After adjustment for covariates, the trend was similar for left ventricular (LV) ejection fraction (Ptrend ≥ 0.07) but significantly worse for GLS, e' and E/e' (Ptrend ≤ 0.02) across the six groups or passing from normal weight to obese individuals irrespective of metabolic status. MHO participants had lower GLS (20.4 vs. 21.4%) and e' (9.6 vs. 10.6 cm/s) compared with controls (P < 0.0001) but had similar GLS (P = 0.47) compared with metabolically unhealthy obese (MUO). Regardless of obesity status, metabolically unhealthy participants had worse diastolic function compared with their metabolically healthy counterparts (P ≤ 0.0004). Compared with controls, MHO individuals were at higher risk of subclinical LV systolic dysfunction (OR = 3.44, 95% CI = 1.25-9.49, P = 0.02). These results were robust to sensitivity analysis.MHO was substantially associated with worse subclinical systolic function although early diastolic dysfunction seemed to be more accentuated in MUO.
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Cardiovascular disease (CVD), principally heart disease and stroke, has become the worldwide leading killer for people of all racial and ethnic groups. In China, this disease contributes 41% to all deaths each year, and it costs the country more than 400 billion US dollars in last decade, including health expenditures and lost productivity, which continues to grow as the population size increases. Recent research findings indicate that CVD can be effectively prevented to some extent by an interdisciplinary approach that combines ICT (Information and Communication Technology) and healthcare applications. Based on this motivation, we developed WE-CARE, a Wearable Efficient teleCARdiology systEm using mobile 7-lead ECG devices. Our WE-CARE system surpasses existing resting ECG systems that reside in hospitals owing to its improved mobility brought by wearable and mobile ECG devices. Meanwhile, it outperforms those conventional dynamic 1-lead or 3-lead ECG systems for mobile users in terms of the appropriate ECG information required for clinical proposes. We carried out clinical trials by deploying the WE-CARE systems at People Hospital of Peking University. The results showed that our solution achieves a high detection rate over 95% against common types of anomalies in ECG signals, while its risk alert delay is limited around one second, both of which match the criteria of real-time healthcare monitoring very well. As demonstrated by the results, the WE-CARE system is a useful and efficient tool for the cardiovascular disease prevention and daily monitoring.
A gas sensor made from graphene vertical field effect transistor (VGr-FET) has been fabricated using graphene as the source electrode, C60 thin film as the semiconductor layer and aluminum thin film as the drain electrode. The on/off ratio of transistor gated by bottom electrode with ionic liquid gel as dielectric layer is derived to be 103 from measured source-drain current I ds. The apparent energy barrier height between the graphene and polycrystalline fullerene was calculated from the model of heterojunction diode I-V response curves. The barrier height φ BH was altered by the gating potential vertically applied on graphene sheet, resulting the large on/off ratio of the transistor. The effect of surface adsorption of water vapor, oxygen, ammonia and isoprene gas phase molecules on the I ds was measured. The lower limit of detection (LOD) for ammonia (86 ppb) than that of isoprene (420 ppb) is attributed to the donor nature of ammonia contact with p-type graphene, and the adsorbed donor leads to a corresponding positive gating effect to the VGr-FET. This facile, low cost and quick responsive device shows promise for early diagnose of severe human respiratory diseases.
BACKGROUND Second hand smoke (SHS), a main indoor air pollutant, is a significant risk factor for cardiovascular morbidity and mortality. We previously showed that exposure to SHS, for as short as four weeks, significantly reduced heart rate variability (HRV), suggesting a decreased vagal regulation of the heart. We further showed that, in cardiac vagal neurons in the nucleus ambiguus (NA), SHS exposure significantly reduced spiking response to depolarizing current injections and increased current‐ and voltage‐threshold for action potential generation. However, we have no information on the effects of SHS exposure on cardiac vagal neurons in the dorsal motor nucleus of vagus (DMNV). Here, we sought to test the hypothesis that SHS exposure decreases neuronal excitability of cardiac vagal neurons in the DMNV. METHODS Seven‐week old male C57BL/6J mice underwent surgeries to retrograde label cardiac vagal neurons by applying a fluorescent dye (DiI) to the sinoatrial node. Two weeks after surgery, mice were randomly assigned to either filtered air‐ (FA, n = 14) or SHS‐exposed (n = 16) group. The SHS exposure (6 hr/d, 5 d/wk) was set at a level that is similar to that of a smoky bar (3 mg/m 3 ). After four weeks of FA or SHS exposure, whole‐cell current clamp recordings in brainstem slices were performed on anatomically identified cardiac vagal neurons in the DMNV with fluorescent labeling. RESULTS DMNV cardiac vagal neurons from the SHS‐exposed group were significantly more hyperpolarized than the FA control group (−53.3 ± 0.9 mV vs. −55.7 ± 0.7 mV, FA vs. SHS respectively, p < 0.05). Four weeks of SHS exposure also significantly decreased neuronal spontaneous spiking activity at a holding potential of −45 mV (1.6 ± 0.4 Hz vs. 0.8 ± 0.2 Hz, FA vs. SHS respectively, p < 0.05). The decreased spontaneous activity was not associated with the spiking response to depolarizing current injections from a holding potential of −60 mV, current and voltage threshold for action potential generation, action potential peak and afterhyperpolarization. Furthermore, there was no significant difference in the neuronal input‐output relationship of DMNV cardiac vagal neurons between FA control and SHS‐exposed groups, suggesting an unchanged dynamic responsiveness to stimuli. CONCLUSIONS Four weeks exposure to environmentally relevant level of SHS decreased neuronal excitability of cardiac vagal neurons in a region‐dependent manner – reduced resting membrane potential and spontaneous spiking activity in the DMNV and reduced spiking response to depolarizing current injections and increased threshold for action potential generation in the NA. Support or Funding Information Funding: R01 ES025229
Abstract Objectives The N-terminal fragment of pro-B-type natriuretic peptide (NT-proBNP) is a widely used heart failure (HF) biomarker. Commercial NT-proBNP immunoassays detect only a subfraction of endogenous NT-proBNP, as the antibodies target a region of NT-proBNP that could be glycosylated at Ser44. The diagnostic utility of immunoassays measuring total NT-proBNP remains unclear. Methods NT-proBNP was measured in 183 HF and 200 non-HF patients diagnosed by two independent cardiologists blinded to NT-proBNP results. Plasma samples either non-treated or treated with a mixture of glycosidases were analyzed by the Elecsys proBNP II assay (Roche Diagnostics, based on antibodies targeting a glycosylated region of NT-proBNP) and the SuperFlex NT-proBNP assay (PerkinElmer, based on antibodies targeting regions of NT-proBNP that are free of O-glycans). The diagnostic accuracy of the two assays was analyzed by comparison of ROC curves. Results The ROC-AUC for the proBNP II assay was 0.943 (95% CI 0.922–0.964) for NT-proBNP measured in untreated samples and 0.935 (0.913–0.958) for NT-proBNP measured in glycosidase-treated samples. The SuperFlex NT-proBNP assay in untreated samples gave a ROC-AUC of 0.930 (95% CI 0.907–0.954). The median percentage of non-glycosylated NT-proBNP to total NT-proBNP was 1.5–1.6-fold lower in the non-HF group compared to that in the HF group. Conclusions The clinical value of total NT-proBNP for HF diagnosis was similar to the subfraction of NT-proBNP that was non-glycosylated at Ser44. The lower percentage of non-glycosylated NT-proBNP to total NT-proBNP in non-HF patients suggests that total NT-proBNP might be more sensitive in individuals without current or prior symptoms of HF.
The cover image is based on the Research Report Comprehensive risk assessments and anesthetic management for children with osteogenesis imperfecta: A retrospective review of 252 orthopedic procedures over 5 years by Xiyun Liang et al., https://doi.org/10.1111/pan.14454.
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