Pulmonary hypertension is a chronic disease developing progressively with high mortality. Pulmonary hypertension patients need persistent medical care; however, limited reports focused on them when there was an outbreak of coronavirus disease 2019 in China. This national survey was aimed to evaluate the overall condition of pulmonary hypertension patients during this period. A questionnaire regarding the living condition of pulmonary hypertension patients during coronavirus disease 2019 was designed by pulmonary hypertension diagnostic experts in Wuhan Asia Heart Hospital. Pulmonary hypertension patients and their family members were invited to participate in this survey online. One-hundred twenty pulmonary hypertension patients and 23 family members participated in the survey; 64.8% ( n = 87) participants came from Hubei, and others were from 15 other provinces; 98.6% ( n = 141) participants were in home quarantine; 65.8% ( n = 79) were pulmonary arterial hypertension associated with congenital heart disease; and 76.7% ( n = 92) patients proclaimed their heart function was well maintained at class I or II. One (0.8%) patient was confirmed severe acute respiratory syndrome coronavirus 2 infection. Two (1.7%) patients were hospitalized due to heart function worsening. Nearly 70% ( n = 100) participants implied shortage in medications during coronavirus disease 2019 outbreak. A total of 24.2% ( n = 29) patients indicated that medications were discontinued due to the insufficient supply. Most of the participants stayed optimistic on either coronavirus disease 2019 outbreak or their pulmonary hypertension disease, and 61.7% ( n = 74) patients would go to the hospital for follow-up immediately after outbreak. These preliminary data show pulmonary hypertension patients are able to avoid severe disease when they are in home quarantine. Medication supplement is important for pulmonary hypertension patients when their heart function is well maintained. In addition, there might be increasing requirements of medical care for pulmonary hypertension patients after the outbreak.
Objective Nonalcoholic fatty liver disease (NAFLD) is a condition associated with type 2 diabetes (T2D). Insulin resistance, a common pathogenesis of NAFLD and T2D, is partially caused by alterations in angiotensin II (Ang II) and is accompanied by hypoadiponectinemia. We aimed to investigate whether the circulating Ang II and adiponectin concentrations are related to hyperglycemia in male NAFLD patients. Methods Thirty-five controls and 85 NAFLD patients without prior known T2D were enrolled. All participants were non-smoking men who performed 75-g oral glucose tolerance tests. According to the American Diabetes Association (ADA) criteria, the NAFLD patients were divided into the euglycemia and hyperglycemia groups. The NAFLD patients with hyperglycemia were further divided into the isolated impaired fasting glucose (I-IFG) and postprandial hyperglycemia subgroups. The fasting serum Ang II and adiponectin concentrations were measured. Results Among the 85 NAFLD patients, 40 (47%) had hyperglycemia, including I-IFG (18%) and postprandial hyperglycemia (29%). The serum Ang II concentrations in the euglycemia and hyperglycemia groups were significantly higher than those observed in the control and euglycemia groups, respectively; whereas the serum adiponectin concentrations were significantly lower. The serum Ang II concentrations were significantly higher in the postprandial hyperglycemia subgroup than in the I-IFG subgroup. The serum Ang II and adiponectin concentrations were found to be independent predictors of hyperglycemia in the NAFLD patients. The serum Ang II concentration was significantly associated with the serum adiponectin and 2-hour postprandial glucose concentrations in the NAFLD patients. Conclusion An increased circulating Ang II concentration is associated with hypoadiponectinemia and postprandial hyperglycemia in male NAFLD patients and may be involved in the pathogenesis of T2D in NAFLD patients.
SummaryWe present a case of an infectious pseudoaneurysm after patent ductus arteriosus (PDA) closure with a ventricular septal defect (VSD) occluder in a two-year-old child. The aneurysm grew rapidly but was successfully removed in time and the patient survived. To our knowledge, this is the first report of an infectious pseudoaneurysm caused by VSD occluder in PDA closure.(Int Heart J 2017; 58: 1017-1019) Key words: Aneurysmal dilatation, Infectious endocarditis, Transcatheter A neurysmal dilatation of ductus arteriosus has been considered a rare but potentially fatal abnormality. It can be either congenital or acquired as a complication of surgical ligation of patent ductus arteriosus (PDA) or after a ductal infection. And the congenital ones were much commoner than the acquired ones. In the early days, the surgical method for PDA was excision, which was replaced by occluder nowadays. There were case reports on ductus arteriosus aneurysm in PDA excision.1,2) However, to our knowledge, this is the first report of pseudoaneurysm caused by PDA occluder. Case ReportA two-year-old girl (weighing 10.5 kg) presented with a week history of cough. A physical examination revealed a continuous murmur at the second left intercostal space. Transthoracic echocardiogram revealed a PDA (Figure 1).The patient underwent right heart catheterization. A 5 French (Fr) sheath was inserted into the right femoral vein, followed by a 5-Fr MPA1 catheter, and right-sided pressures were recorded. The catheter was removed, flushed, and then inserted into the right femoral artery. The left-sided pressures were then recorded.The patient was found to have a funnel-shaped PDA (5 mm pulmonary end diameter, 13 mm aortic end diameter and 8 mm length) with preprocedural shunt and Qp:Qs of 4.1:1 (Figure 2). Right heart catheterization demonstrated a pulmonary arterial pressure of 90 mmHg/50 mmHg (mean 63 mmHg) with a mean pulmonary capillary wedge pressure of 7 mmHg. The pulmonary vessel resistance was 459 dynes sec cm-5.A 14 mm muscular ventricular septal defect (mVSD) occluder (Starway Medical Technology, China) was advanced to the site of the PDA through a 9 Fr delivery system. Its subsequent deployment closed the PDA. Postprocedural pulmonary arterial pressure was recorded as 50 mmHg/30 mmHg (mean 37 mmHg). Postoperative transthoracic echocardiogram (TTE) found no residual shunt. 0.5 g Cefazolin was given prophylactically 40 minutes before the procedure and 11.5 hours after the procedure. The postoperative examinations were normal and the patient was discharged. However, the patient came down with a fever of 40 15 days after the procedure and was transferred from a local hospital to ours. The high fever has been lasting and no response for medicines with Vancomycin and Meropenem for 2 weeks at local hospital. TTE showed that the occluder seemed to drop into the main pulmonary artery. The cardiac computed tomographic angiography revealed an aneurysmal dilatation of the ductus arteriosus with a maximum diameter of 30 mm (Figure 3, 28*30 mm). The...
Background Pediatric patients with genetic disorders have a higher incidence of pulmonary arterial hypertension (PAH) regardless of their heart defects. Filamin A (FLNA) mutation is recently recognized to be associated with pediatric pulmonary disorders, however, the clinical courses of PAH related to the mutation were reported in limited cases. Here, we presented a case and pooled data for better understanding of the correlation between FLNA mutation and pediatric PAH. Case presentation The patient was a 8-month-old female with repeated episodes of pneumonia. Physical examination revealed cleft lip, cleft palate and developmental retardation. Imaging examination showed a small atrial septal defect (ASD), central pulmonary artery enlargement, left upper lobe of lung atelectasis, and pulmonary infiltration. Genetic test showed she carried a de novo pathogenic variant of FLNA gene (c.5417-1G > A, p.-). Oral medications didn’t slow the progression of PAH in the patient, and she died two years later. Conclusions FLNA mutation causes rare but progressive PAH in addition to a wide spectrum of congenital heart disease and other comorbidities in pediatric patients. We highly recommend genetic testing for pediatric patients when suspected with PAH. Given the high mortality in this group, lung transplantation may offer a better outcome.
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